Journal articles on the topic 'R Injury'
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1
Campbell, Thomas F., Christine Dollaghan, Janine Janosky, Heather Leavy Rusiewicz, Steven L. Small, Frederic Dick, Jennell Vick, and P. David Adelson. "Consonant Accuracy After Severe Pediatric Traumatic Brain Injury: A Prospective Cohort Study." Journal of Speech, Language, and Hearing Research 56, no. 3 (June 2013): 1023–34. http://dx.doi.org/10.1044/1092-4388(2012/12-0077).
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Purpose The authors sought to describe longitudinal changes in Percentage of Consonants Correct—Revised (PCC–R) after severe pediatric traumatic brain injury (TBI), to compare the odds of normal-range PCC–R in children injured at older and younger ages, and to correlate predictor variables and PCC–R outcomes. Method In 56 children injured between age 1 month and 11 years, PCC–R was calculated over 12 monthly sessions beginning when the child produced ≥ 10 words. At each session, the authors compared odds of normal-range PCC–R in children injured at younger (≤ 60 months) and older (> 60 months) ages. Correlations were calculated between final PCC–R and age at injury, injury mechanism, gender, maternal education, residence, treatment, Glasgow Coma Score, and intact brain volume. Results PCC–Rs varied within and between children. Odds of normal-range PCC–R were significantly higher for the older than for the younger group at all sessions but the first; odds of normal-range PCC–R were 9 to 33 times higher in the older group in sessions 3 to 12. Age at injury was significantly correlated with final PCC–R. Conclusion Over a 12-month period, severe TBI had more adverse effects for children whose ages placed them in the most intensive phase of PCC–R development than for children injured later.
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Kuboki, Satoshi, Nozomu Sakai, Johannes Tschöp, Michael J. Edwards, Alex B. Lentsch, and Charles C. Caldwell. "Distinct contributions of CD4+ T cell subsets in hepatic ischemia/reperfusion injury." American Journal of Physiology-Gastrointestinal and Liver Physiology 296, no. 5 (May 2009): G1054—G1059. http://dx.doi.org/10.1152/ajpgi.90464.2008.
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Helper T cells are known to mediate hepatic ischemia/reperfusion (I/R) injury. However, the precise mechanisms and subsets of CD4+ T cells that contribute to this injury are still controversial. Therefore, we sought to determine the contributions of different CD4+ T cell subsets during hepatic I/R injury. Wild-type, OT-II, or T cell receptor (TCR)-δ-deficient mice were subjected to 90 min of partial hepatic ischemia followed by 8 h of reperfusion. Additionally, wild-type mice were pretreated with anti-CD1d, -NK1.1, or -IL-2R-α antibodies before I/R injury. OT-II mice had diminished liver injury compared with wild-type mice, implicating that antigen-dependent activation of CD4+ T cells through TCRs is involved in hepatic I/R injury. TCR-δ knockout mice had decreased hepatic neutrophil accumulation, suggesting that γδ T cells regulate neutrophil recruitment. We found that natural killer T (NKT) cells, but not NK cells, contribute to hepatic I/R injury via CD1d-dependent activation of their TCRs, as depletion of NKT cells by anti-CD1d antibody or depletion of both NKT cells and NK cells by anti-NK1.1 attenuated liver injury. Although regulatory T cells (Treg) are known to suppress T cell-dependent inflammation, depletion of Treg cells had little effect on hepatic I/R injury. The data suggest that antigen-dependent activation of CD4+ T cells contributes to hepatic I/R injury. Among the subsets of CD4+ T cells, it appears that γδ T cells contribute to neutrophil recruitment and that NKT cells directly injure the liver. In contrast, NK cells and Treg have little effects on hepatic I/R injury.
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Lu, Ping, Shihui Xiao, Shaoze Chen, Youlin Fu, Peng Zhang, Yaner Yao, and Feng Chen. "LncRNA SNHG12 downregulates RAGE to attenuate hypoxia-reoxygenation-induced apoptosis in H9c2 cells." Bioscience, Biotechnology, and Biochemistry 85, no. 4 (February 3, 2021): 866–73. http://dx.doi.org/10.1093/bbb/zbaa090.
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ABSTRACT Ischemia-reperfusion (I/R) injury causes cardiac dysfunction through several mechanisms including the irregular expression of some long noncoding RNA. However, the role of SNHG12 in myocardial I/R injury remains unclear. Here, we found the increase of the SNHG12 level in hypoxia-reoxygenation (H/R)-injured-H9c2 cells. SNHG12 silencing enhanced the apoptosis of H/R-injured H9c2 cells, while SNHG12 overexpression relieved the cardiomyocyte apoptosis induced by H/R stimulation. Additionally, the suppression of SNHG12 significantly boosted the H/R-induced expression and the production of TNF-α, IL-6, and IL-1β, as well as the activation of NF-κB, which were fully reversed after overexpression of SNHG12. Mechanistically, SNHG12 adversely regulated the production of receptor for advanced glycation end products (RAGE) in H/R-stimulated H9c2 cells. Antibody blocking of RAGE alleviated the apoptosis of H/R-injured H9c2 cells. Collectively, we have determined a valuable mechanism by which the high level of SNHG12 contributes to H9c2 cells against H/R injury through the reduction of RAGE expression.
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Miyake, Hiromasa, Katsuyuki Tanabe, Satoshi Tanimura, Yuri Nakashima, Tomoyo Morioka, Kana Masuda, Hitoshi Sugiyama, Yasufumi Sato, and Jun Wada. "Genetic Deletion of Vasohibin-2 Exacerbates Ischemia-Reperfusion-Induced Acute Kidney Injury." International Journal of Molecular Sciences 21, no. 12 (June 26, 2020): 4545. http://dx.doi.org/10.3390/ijms21124545.
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Acute kidney injury (AKI) has been increasingly recognized as a risk factor for transition to chronic kidney disease. Recent evidence suggests that endothelial damage in peritubular capillaries can accelerate the progression of renal injury. Vasohibin-2 (VASH2) is a novel proangiogenic factor that promotes tumor angiogenesis. However, the pathophysiological roles of VASH2 in kidney diseases remain unknown. In the present study, we examined the effects of VASH2 deficiency on the progression of ischemia–reperfusion (I/R) injury-induced AKI. I/R injury was induced by bilaterally clamping renal pedicles for 25 min in male wild-type (WT) and Vash2 homozygous knockout mice. Twenty-four hours later, I/R injury-induced renal dysfunction and tubular damage were more severe in VASH2-deficient mice than in WT mice, with more prominent neutrophil infiltration and peritubular capillary loss. After induction of I/R injury, VASH2 expression was markedly increased in injured renal tubules. These results suggest that VASH2 expression in renal tubular epithelial cells might be essential for alleviating I/R injury-induced AKI, probably through protecting peritubular capillaries and preventing inflammatory infiltration.
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Edwards, Jessica K. "New antagonist prevents I/R injury." Nature Reviews Nephrology 11, no. 11 (September 29, 2015): 631. http://dx.doi.org/10.1038/nrneph.2015.161.
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Song, Ying, Weihai Liu, Yi Ding, Yanyan Jia, Jinyi Zhao, Fan Wang, Juan Bai, et al. "Salvianolic acid A ameliorates renal ischemia/reperfusion injury by activating Akt/mTOR/4EBP1 signaling pathway." American Journal of Physiology-Renal Physiology 315, no. 2 (August 1, 2018): F254—F262. http://dx.doi.org/10.1152/ajprenal.00508.2017.
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Salvianolic acid A (Sal A) has been shown to prevent and treat ischemic cardiovascular, as well as cerebral vascular diseases. However, little is known about Sal A in renal ischemia/reperfusion (I/R) injury. In this study, a renal I/R injury model in rats and a hypoxia/reoxygenation (H/R) model to damage proximal renal tubular cells (HK-2) were used to assess whether Sal A halts the development and progression of renal I/R injury. As compared with vehicle treatment, Sal A significantly attenuated kidney injury after renal I/R injury, accompanied by decreases in plasma creatinine, blood urea nitrogen levels, the number of apoptosis-positive tubular cells, and kidney oxidative stress. Sal A also activated phosphorylated protein kinase B (p-Akt) and phosphorylated-mammalian target of rapamycin (p-mTOR) compared with vehicle-treated I/R injury rats. In H/R-injured HK-2 cells, Sal A can reduce the levels of reactive oxygen species in a dose-related manner. Similar to the results from in vivo experiments, in vitro Sal A also increased the protein expression of phosphorylated-eukaryotic initiation factor 4E binding protein 1 (p-4EBP1) compared with vehicle. Furthermore, the cytoprotective activity of Sal A was inhibited by LY294002 and rapamycin. These findings indicate that Sal A can ameliorate renal I/R injury and promote tubular cell survival partly via the Akt/mTOR/4EBP1pathway. Sal A could be a candidate compound to prevent ischemic tissue damage.
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Hu, Yongjun, Hongwei Pan, Jianqiang Peng, Jin He, Mingxiang Tang, Sulan Yan, Jingjing Rong, et al. "Resveratrol inhibits necroptosis by mediating the TNF-α/RIP1/RIP3/MLKL pathway in myocardial hypoxia/reoxygenation injury." Acta Biochimica et Biophysica Sinica 53, no. 4 (March 4, 2021): 430–37. http://dx.doi.org/10.1093/abbs/gmab012.
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Abstract Resveratrol (RES) protects myocardial cells from hypoxia/reoxygenation (H/R)-caused injury. However, the mechanism of this effect has not been clarified. Thus, in this study, we aimed to determine whether RES attenuates H/R-induced cell necroptosis by inhibiting the tumor necrosis factor-alpha (TNF-α)/receptor-interacting protein kinase 1 (RIP1)/RIP3/mixed-lineage kinase domain-like (MLKL) signaling pathway. Rat myocardial ischemia/reperfusion (I/R) models and H/R-injured cell models were constructed. Our study showed that myocardial H/R injury significantly increased the levels of TNF-α, RIP1, RIP3, and p-MLKL/MLKL by western blot analysis. Cell viability assay and 4,6-dianmidino-2-phenylindole (DAPI)–propidium iodide staining showed that the cell viability was decreased, and necroptosis was increased after myocardial H/R injury. The expressions of TNF-α, RIP1, RIP3, and p-MLKL/MLKL in H/R myocardial cells treated with different concentrations of RES were significantly downregulated. In addition, we also found that the cell viability was increased and necroptosis was decreased in dose-dependent manners when H/R-injured cells were treated with RES. In addition, the enhanced effect of TNF-α on necroptosis in myocardial H/R-injured cells was improved by RES, and the effect of RES was confirmed in vivo in I/R rats. This study also showed that RES suppresses necroptosis in H9c2 cells, which may occur through the inhibition of the TNF-α/RIP1/RIP3/MLKL signaling pathway. Our data suggest that necroptosis is a promising therapeutic target and may be a promising therapeutic target for the treatment of myocardial I/R injury.
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Neely, C. F., and I. M. Keith. "A1 adenosine receptor antagonists block ischemia-reperfusion injury of the lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 268, no. 6 (June 1, 1995): L1036—L1046. http://dx.doi.org/10.1152/ajplung.1995.268.6.l1036.
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Ischemia-reperfusion (I-R) injury of the lung occurs after lung transplantation, pulmonary thromboembolectomy, or cardiopulmonary bypass. In the heart, adenosine, A1 adenosine receptor agonists, and a brief period of preconditioning ischemia attenuate I-R injury. Moreover, in the lung, thromboxane is released during ischemia and is an important mediator of I-R injury. We previously reported that adenosine produces vasoconstriction in the feline pulmonary vascular bed by acting on A1 receptors to induce the release of thromboxane and that these vasoconstrictor responses are desensitized by low doses of A1 receptor agonists. Because A1 receptor agonists mimic the effect of preconditioning ischemia, we hypothesized, in contrast to previously proposed mechanisms, that small amounts of adenosine released during preconditioning ischemia desensitize A1 receptors. Also, we hypothesized that greater amounts of adenosine are released after longer periods of ischemia, which activate A1 receptors. Thus if desensitization of A1 receptors is the mechanism by which preconditioning attenuates I-R injury of the heart and A1 receptor activation during ischemia plays an important role in I-R injury of the lung, A1 receptor antagonists should provide a protective effect in I-R injury of the lung. In this study, 2 h of ischemia and 2 h of reperfusion of the left lower lobe in intact-chest, spontaneously breathing cats caused lung injury characterized by the presence of neutrophils, macrophages, and RBCs in alveoli and caused alveolar edema, which was blocked in a highly significant manner by the A1 receptor antagonists xanthine amine congener (XAC) and 1,3-dipropyl-8-cyclopentylxanthine (DPCPX). An intralobar arterial infusion of XAC (30 min before ischemia) reduced the %injured alveoli (defined as presence of 2 or more inflammatory cells or RBCs, or edematous fluid) from 60 +/- 10 to 7 +/- 2%, which was not significantly different from controls (5 +/- 1%; P < 0.0001). DPCPX (iv) reduced the %injured alveoli to 13 +/- 7% when administered 30 min before ischemia and to 6 +/- 2% when administered after 1 h of reperfusion, not significantly different from controls (P < 0.0001). Preconditioning ischemia (10-min ischemia +10-min reperfusion) also reduced the %injured alveoli after 2 h ischemia and 2 h reperfusion to 23 +/- 13%, almost identical to 2 h ischemia and 1 h reperfusion. These data support the hypothesis that A1 receptor antagonists block I-R injury of the lung. A1 receptor antagonists may be useful in preventing I-R injury after transplant surgery and during surgical procedures associated with I-R injury of the heart, brain, kidney, and spinal cord.
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Sprague, Christy L., Donald Penner, and James J. Kells. "Enhancing the margin of selectivity of RPA 201772 inZea mayswith antidotes." Weed Science 47, no. 5 (October 1999): 492–97. http://dx.doi.org/10.1017/s004317450009216x.
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The antidotes dichlormid, MON-4660, CGA-154281, R-29148, and MON-13900 were tested in the greenhouse to protectZea maysL. (corn) against RPA 201772 injury. High rates of RPA 201772 injured four Z.mayshybrids > 30%. R-29148 and MON-13900 were the most effective of the five antidotes evaluated. R-29148 applied at rates ⩾ 45 g ha−1provided excellent protection against RPA 201772 injury and also prevented injury toZ. maysfrom diketonitrile, the active metabolite of RPA 201772. In laboratory studies, R-29148 did not alter absorption of14C-RPA 201772 from soil; however, R-29148 significantly enhanced the rate of RPA 201772 metabolism and inactivation inZ. mays.The mixed function oxidase inhibitor piperonyl butoxide (PBO) increased RPA 201772 injury on all hybrids. These results demonstrate thatZ. maystolerance to RPA 201772 can be enhanced with the use of antidotes such as R-29148 and MON-13900, that R-29148 protectsZ. maysfrom RPA 201772 and diketonitrile by the enhancement of metabolism, and that oxidative reactions may be involved in the metabolism of RPA 201772 inZ. mays.
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Meng, X., M. Wei, D. Wang, X. Qu, K. Zhang, N. Zhang, and Xinjian Li. "The protective effect of hesperidin against renal ischemia-reperfusion injury involves the TLR-4/NF-κB/iNOS pathway in rats." Physiology International 107, no. 1 (March 2020): 82–91. http://dx.doi.org/10.1556/2060.2020.00003.
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AbstractRenal injury is reported to have a high mortality rate. Additionally, there are several limitations to current conventional treatments that are used to manage it. This study evaluated the protective effect of hesperidin against ischemia/reperfusion (I/R)-induced kidney injury in rats. Renal injury was induced by generating I/R in kidney tissues. Rats were then treated with hesperidin at a dose of 10 or 20 mg/kg intravenously 1 day after surgery for a period of 14 days. The effect of hesperidin on renal function, serum mediators of inflammation, and levels of oxidative stress in renal tissues were observed in rat kidney tissues after I/R-induced kidney injury. Moreover, protein expression and mRNA expression in kidney tissues were determined using Western blotting and RT-PCR. Hematoxylin and eosin (H&E) staining was done for histopathological observation of kidney tissues. The data suggest that the levels of blood urea nitrogen (BUN) and creatinine in the serum of hesperidin-treated rats were lower than in the I/R group. Treatment with hesperidin also ameliorated the altered level of inflammatory mediators and oxidative stress in I/R-induced renal-injured rats. The expression of p-IκBα, caspase-3, NF-κB p65, Toll-like receptor 4 (TLR-4) protein, TLR-4 mRNA, and inducible nitric oxide synthase (iNOS) was significantly reduced in the renal tissues of hesperidin-treated rats. Histopathological findings also revealed that treatment with hesperidin attenuated the renal injury in I/R kidney-injured rats. In conclusion, our results suggest that hesperidin protects against renal injury induced by I/R by involving TLR-4/NF-κB/iNOS signaling.
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Jin, Younggeon, and Anthony T. Blikslager. "Myosin light chain kinase mediates intestinal barrier dysfunction via occludin endocytosis during anoxia/reoxygenation injury." American Journal of Physiology-Cell Physiology 311, no. 6 (December 1, 2016): C996—C1004. http://dx.doi.org/10.1152/ajpcell.00113.2016.
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Intestinal anoxia/reoxygenation (A/R) injury induces loss of barrier function followed by epithelial repair. Myosin light chain kinase (MLCK) has been shown to alter barrier function via regulation of interepithelial tight junctions, but has not been studied in intestinal A/R injury. We hypothesized that A/R injury would disrupt tight junction barrier function via MLCK activation and myosin light chain (MLC) phosphorylation. Caco-2BBe1 monolayers were subjected to anoxia for 2 h followed by reoxygenation in 21% O2, after which barrier function was determined by measuring transepithelial electrical resistance (TER) and FITC-dextran flux. Tight junction proteins and MLCK signaling were assessed by Western blotting, real-time PCR, or immunofluorescence microscopy. The role of MLCK was further investigated with select inhibitors (ML-7 and peptide 18) by using in vitro and ex vivo models. Following A/R injury, there was a significant increase in paracellular permeability compared with control cells, as determined by TER and dextran fluxes ( P < 0.05). The tight junction protein occludin was internalized during A/R injury and relocalized to the region of the tight junction after 4 h of recovery. MLC phosphorylation was significantly increased by A/R injury ( P < 0.05), and treatment with the MLCK inhibitor peptide 18 attenuated the increased epithelial monolayer permeability and occludin endocytosis caused by A/R injury. Application of MLCK inhibitors to ischemia-injured porcine ileal mucosa induced significant increases in TER and reduced mucosal-to-serosal fluxes of3H-labeled mannitol. These data suggest that MLCK-induced occludin endocytosis mediates intestinal epithelial barrier dysfunction during A/R injury. Our results also indicate that MLCK-dependent occludin regulation may be a target for the therapeutic treatment of ischemia/reperfusion injury.
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Yu, Haijie, Haishan Zhang, Weihua Zhao, Liang Guo, Xueyuan Li, Yang Li, Xingang Zhang, and Yingxian Sun. "Gypenoside Protects against Myocardial Ischemia-Reperfusion Injury by Inhibiting Cardiomyocytes Apoptosis via Inhibition of CHOP Pathway and Activation of PI3K/Akt Pathway In Vivo and In Vitro." Cellular Physiology and Biochemistry 39, no. 1 (2016): 123–36. http://dx.doi.org/10.1159/000445611.
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Background/Aims: Ischemia-reperfusion (I/R) injury is believed to be the major cause for detriments in coronary heart diseases, but few effective therapies for prevention or treatment of I/R injury are available. Gypenoside (GP) is the predominant effective component of Gynostemma pentaphyllum and possesses capacities against inflammation and oxidation. In the present study, the role of GP in ameliorating myocardial I/R injury was investigated. Methods: effect GP on the cardiac structure of I/R injured rats was assessed by H&E and TTC staining. Then the influence of GP on the cardiac function of rat model was determined by measuring hemodynamics parameters, levels of lactate dehydrogenase (LDH) and creatine kinase (CK). Thereafter, effect of GP on apoptotic process was evaluated with both rat and cell models. The production of molecules related to ER stress and apoptosis was quantified for revelation of pathways involved in the myocardial protective effect of GP. Results: Impairments in cardiac structure due to I/R injury was ameliorated by GP treatment. And it was evidently demonstrated that administration of GP not only effectively decreased the apoptotic rates in both rat and cell models but also markedly improved the cardiac function of I/R injured rats. In addition, results of western blotting revealed that the GP inhibited ER-stress and apoptosis through the blockade of CHOP pathway and activation of PI3K/Akt pathway. Conclusion: the current study showed the potential of GP to alleviate myocardial I/R injury and preliminarily uncovered the underling mechanism driving this treatment.
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Ascher, Stefanie, Eivor Wilms, Giulia Pontarollo, Henning Formes, Franziska Bayer, Maria Müller, Frano Malinarich, et al. "Gut Microbiota Restricts NETosis in Acute Mesenteric Ischemia-Reperfusion Injury." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 9 (September 2020): 2279–92. http://dx.doi.org/10.1161/atvbaha.120.314491.
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Objective: Recruitment of neutrophils and formation of neutrophil extracellular traps (NETs) contribute to lethality in acute mesenteric infarction. To study the impact of the gut microbiota in acute mesenteric infarction, we used gnotobiotic mouse models to investigate whether gut commensals prime the reactivity of neutrophils towards formation of neutrophil extracellular traps (NETosis). Approach and Results: We applied a mesenteric ischemia-reperfusion (I/R) injury model to germ-free (GF) and colonized C57BL/6J mice. By intravital imaging, we quantified leukocyte adherence and NET formation in I/R-injured mesenteric venules. Colonization with gut microbiota or monocolonization with Escherichia coli augmented the adhesion of leukocytes, which was dependent on the TLR4 (Toll-like receptor-4)/TRIF (TIR-domain–containing adapter-inducing interferon-β) pathway. Although neutrophil accumulation was decreased in I/R-injured venules of GF mice, NETosis following I/R injury was significantly enhanced compared with conventionally raised mice or mice colonized with the minimal microbial consortium altered Schaedler flora. Also ex vivo, neutrophils from GF and antibiotic-treated mice showed increased LPS (lipopolysaccharide)-induced NETosis. Enhanced TLR4 signaling in GF neutrophils was due to elevated TLR4 expression and augmented IRF3 (interferon regulatory factor-3) phosphorylation. Likewise, neutrophils from antibiotic-treated conventionally raised mice had increased NET formation before and after ischemia. Increased NETosis in I/R injury was abolished in conventionally raised mice deficient in the TLR adaptor TRIF. In support of the desensitizing influence of enteric LPS, treatment of GF mice with LPS via drinking water diminished LPS-induced NETosis in vitro and in the mesenteric I/R injury model. Conclusions: Collectively, our results identified that the gut microbiota suppresses NETing neutrophil hyperreactivity in mesenteric I/R injury, while ensuring immunovigilance by enhancing neutrophil recruitment.
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Konishi, Takanori, Rebecca M. Schuster, and Alex B. Lentsch. "Liver repair and regeneration after ischemia-reperfusion injury is associated with prolonged fibrosis." American Journal of Physiology-Gastrointestinal and Liver Physiology 316, no. 3 (March 1, 2019): G323—G331. http://dx.doi.org/10.1152/ajpgi.00154.2018.
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Liver recovery after hepatic ischemia-reperfusion (I/R) injury is characterized by clearance of dead tissue and its replacement with functional liver parenchyma. Previous reports have observed fibrosis after liver I/R. To determine whether liver fibrosis after I/R was a pathologic consequence of the injury response, we assessed the development of liver fibrosis after I/R and its impact on subsequent insult. A murine model of partial I/R was used to induce liver injury and study the reparative response. During liver remodeling after I/R, expression of the profibrotic genes increased in the ischemic liver. Histologically, α-smooth muscle actin (α-SMA)-positive hepatic stellate cells (HSCs)/myofibroblasts increased, and collagen deposition was enhanced along the injured site. Selective staining experiments showed that HSCs, not portal fibroblasts, were the major source of myofibroblasts. During liver repair after I/R, liver fibrosis was readily observed at the interface between necrotic tissue and regenerating liver in association with HSCs/myofibroblasts. The number of HSCs/myofibroblasts decreasing shortly after the full resolution of necrotic injury and restoration are normal liver architecture. However, liver fibrosis persisted for several more weeks before gradually resolving. Resolution of liver fibrosis was accompanied by upregulated expression of matrix metalloproteinase-13. After resolution of fibrosis, the administration of CCl4 did not result in exacerbated liver injury, suggesting that I/R injury does not predispose the liver to future fibrotic insults. The data suggest that liver fibrosis is a component of tissue repair after I/R, is caused by myofibroblasts derived from HSC, and does not increase susceptibility of the liver to subsequent hepatic injury. NEW & NOTEWORTHY This study is the first to assess pathology of liver fibrosis during the reparative process after ischemia-reperfusion (I/R) injury. Here we show that profibrotic gene expression increased in the liver after I/R, and collagen accumulation produced by hepatic stellate cells (HSCs)/myofibroblasts enhanced at the interface between necrotic tissue and regenerating liver. Liver fibrosis gradually resolved concomitant with decreasing activation of HSC and upregulating matrix metalloproteinase-13. After resolution of fibrosis, the liver was not more susceptible to subsequent hepatic injury.
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Lim, Songhyun, Tae Jung Kim, Young-Ju Kim, Cheesue Kim, Sang-Bae Ko, and Byung-Soo Kim. "Senolytic Therapy for Cerebral Ischemia-Reperfusion Injury." International Journal of Molecular Sciences 22, no. 21 (November 4, 2021): 11967. http://dx.doi.org/10.3390/ijms222111967.
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Ischemic stroke is one of the leading causes of death, and even timely treatment can result in severe disabilities. Reperfusion of the ischemic stroke region and restoration of the blood supply often lead to a series of cellular and biochemical consequences, including generation of reactive oxygen species (ROS), expression of inflammatory cytokines, inflammation, and cerebral cell damage, which is collectively called cerebral ischemia-reperfusion (IR) injury. Since ROS and inflammatory cytokines are involved in cerebral IR injury, injury could involve cellular senescence. Thus, we investigated whether senolytic therapy that eliminates senescent cells could be an effective treatment for cerebral IR injury. To determine whether IR induces neural cell senescence in vitro, astrocytes were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R). OGD/R induced astrocyte senescence and senescent cells in OGD/R-injured astrocytes were effectively eliminated in vitro by ABT263, a senolytic agent. IR in rats with intraluminal middle cerebral artery occlusion induced cellular senescence in the ischemic region. The senescent cells in IR-injured rats were effectively eliminated by intravenous injections of ABT263. Importantly, ABT263 treatment significantly reduced the infarct volume and improved neurological function in behavioral tests. This study demonstrated, for the first time, that senolytic therapy has therapeutic potential for cerebral IR injury.
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Mongkolpathumrat, Podsawee, Anusak Kijtawornrat, Eakkapote Prompunt, Aussara Panya, Nipon Chattipakorn, Stephanie Barrère-Lemaire, and Sarawut Kumphune. "Post-Ischemic Treatment of Recombinant Human Secretory Leukocyte Protease Inhibitor (rhSLPI) Reduced Myocardial Ischemia/Reperfusion Injury." Biomedicines 9, no. 4 (April 13, 2021): 422. http://dx.doi.org/10.3390/biomedicines9040422.
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Myocardial ischemia/reperfusion (I/R) injury is a major cause of mortality and morbidity worldwide. Among factors contributing to I/R injury, proteolytic enzymes could also cause cellular injury, expand the injured area and induce inflammation, which then lead to cardiac dysfunction. Therefore, protease inhibition seems to provide therapeutic benefits. Previous studies showed the cardioprotective effect of secretory leukocyte protease inhibitor (SLPI) against myocardial I/R injury. However, the effect of a post-ischemic treatment with SLPI in an in vivo I/R model has never been investigated. In the present study, recombinant human (rh) SLPI (rhSLPI) was systemically injected during coronary artery occlusion or at the onset of reperfusion. The results show that post-ischemic treatment with rhSLPI could significantly reduce infarct size, Lactate Dehydrogenase (LDH) and Creatine kinase-MB (CK-MB) activity, inflammatory cytokines and protein carbonyl levels, as well as improving cardiac function. The cardioprotective effect of rhSLPI is associated with the attenuation of p38 MAPK phosphorylation, Bax, caspase-3 and -8 protein levels and enhancement of pro-survival kinase Akt and ERK1/2 phosphorylation. In summary, this is the first report showing the cardioprotective effects against myocardial I/R injury of post-ischemic treatments with rhSLPI in vivo. Thus, these results suggest that SLPI could be used as a novel therapeutic strategy to reduce myocardial I/R injury.
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Dos’Santos, Thomas, Christopher Thomas, Alistair McBurnie, Paul Comfort, and Paul A. Jones. "Biomechanical Determinants of Performance and Injury Risk During Cutting: A Performance-Injury Conflict?" Sports Medicine 51, no. 9 (April 3, 2021): 1983–98. http://dx.doi.org/10.1007/s40279-021-01448-3.
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Abstract Background Most cutting biomechanical studies investigate performance and knee joint load determinants independently. This is surprising because cutting is an important action linked to performance and non-contact anterior cruciate ligament (ACL) injuries. The aim of this study was to investigate the relationship between cutting biomechanics and cutting performance (completion time, ground contact time [GCT], exit velocity) and surrogates of non-contact ACL injury risk (knee abduction [KAM] and internal rotation [KIRM] moments) during 90° cutting. Design Mixed, cross-sectional study following an associative design. 61 males from multidirectional sports performed six 90° pre-planned cutting trials, whereby lower-limb and trunk kinetics and kinematics were evaluated using three-dimensional (3D) motion and ground reaction force analysis over the penultimate (PFC) and final foot contact (FFC). Pearson’s and Spearman’s correlations were used to explore the relationships between biomechanical variables and cutting performance and injury risk variables. Stepwise regression analysis was also performed. Results Faster cutting performance was associated (p ≤ 0.05) with greater centre of mass (COM) velocities at key instances of the cut (r or ρ = 0.533–0.752), greater peak and mean propulsive forces (r or ρ = 0.449–0.651), shorter FFC GCTs (r or ρ = 0.569–0.581), greater FFC and PFC braking forces (r = 0.430–0.551), smaller hip and knee flexion range of motion (r or ρ = 0.406–0.670), greater knee flexion moments (KFMs) (r = 0.482), and greater internal foot progression angles (r = − 0.411). Stepwise multiple regression analysis revealed that exit velocity, peak resultant propulsive force, PFC mean horizontal braking force, and initial foot progression angle together could explain 64% (r = 0.801, adjusted 61.6%, p = 0.048) of the variation in completion time. Greater peak KAMs were associated with greater COM velocities at key instances of the cut (r or ρ = − 0.491 to − 0.551), greater peak knee abduction angles (KAA) (r = − 0.468), and greater FFC braking forces (r = 0.434–0.497). Incidentally, faster completion times were associated with greater peak KAMs (r = − 0.412) and KIRMs (r = 0.539). Stepwise multiple regression analysis revealed that FFC mean vertical braking force and peak KAA together could explain 43% (r = 0.652, adjusted 40.6%, p < 0.001) of the variation peak KAM. Conclusion Techniques and mechanics associated with faster cutting (i.e. faster COM velocities, greater FFC braking forces in short GCTs, greater KFMs, smaller hip and knee flexion, and greater internal foot progression angles) are in direct conflict with safer cutting mechanics (i.e. reduced knee joint loading, thus ACL injury risk), and support the “performance-injury conflict” concept during cutting. Practitioners should be conscious of this conflict when instructing cutting techniques to optimise performance while minimising knee joint loading, and should, therefore, ensure that their athletes have the physical capacity (i.e. neuromuscular control, co-contraction, and rapid force production) to tolerate and support the knee joint loading during cutting.
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Jiang, Hailun, Jianguo Xing, Jiansong Fang, Linlin Wang, Yu Wang, Li Zeng, Zhuorong Li, and Rui Liu. "Tilianin Protects against Ischemia/Reperfusion-Induced Myocardial Injury through the Inhibition of the Ca2+/Calmodulin-Dependent Protein Kinase II-Dependent Apoptotic and Inflammatory Signaling Pathways." BioMed Research International 2020 (October 9, 2020): 1–18. http://dx.doi.org/10.1155/2020/5939715.
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Tilianin is a naturally occurring phenolic compound with a cardioprotective effect against myocardial ischemia/reperfusion injury (MIRI). The aim of our study was to determine the potential targets and mechanism of action of tilianin against cardiac injury induced by MIRI. An in silico docking model was used in this study for binding mode analysis between tilianin and Ca2+/calmodulin-dependent protein kinase II (CaMKII). Oxygen-glucose deprivation/reperfusion- (OGD/R-) injured H9c2 cardiomyocytes and ischemia/reperfusion- (I/R-) injured isolated rat hearts were developed as in vitro and ex vivo models, respectively, which were both treated with tilianin in the absence or presence of a specific CaMKII inhibitor KN93 for target verification and mechanistic exploration. Results demonstrated the ability of tilianin to facilitater the recovery of OGD/R-induced cardiomyocyte injury and the maintenance of cardiac function in I/R-injured hearts. Tilianin interacted with CaMKIIδ with an efficient binding performance, a favorable binding score, and restraining p-CaMKII and ox-CaMKII expression in cardiomyocytes injured by MIRI. Importantly, inhibition of CaMKII abolished tilianin-mediated recovery of OGD/R-induced cardiomyocyte injury and maintenance of cardiac function in I/R-injured hearts, accompanied by the disability to protect mitochondrial function. Furthermore, the protective effects of tilianin towards mitochondrion-associated proapoptotic and antiapoptotic protein counterbalance and c-Jun N-terminal kinase (JNK)/nuclear factor- (NF-) κB-related inflammation suppression were both abolished after pharmacological inhibition of CaMKII. Our investigation indicated that the inhibition of CaMKII-mediated mitochondrial apoptosis and JNK/NF-κB inflammation might be considered as a pivotal mechanism used by tilianin to exert its protective effects on MIRI cardiac damage.
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Li, Xinye, Ning Ma, Juping Xu, Yanchi Zhang, Pan Yang, Xin Su, Yanfeng Xing, et al. "Targeting Ferroptosis: Pathological Mechanism and Treatment of Ischemia-Reperfusion Injury." Oxidative Medicine and Cellular Longevity 2021 (October 28, 2021): 1–14. http://dx.doi.org/10.1155/2021/1587922.
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Ischemia-reperfusion (I/R) is a pathological process that occurs in many organs and diseases. Reperfusion, recovery of blood flow, and reoxygenation often lead to reperfusion injury. Drug therapy and early reperfusion therapy can reduce tissue injury and cell necrosis caused by ischemia, leading to irreversible I/R injury. Ferroptosis was clearly defined in 2012 as a newly discovered iron-dependent, peroxide-driven, nonapoptotic form of regulated cell death. Ferroptosis is considered the cause of reperfusion injury. This discovery provides new avenues for the recognition and treatment of diseases. Ferroptosis is a key factor that leads to I/R injury and organ failure. Given the important role of ferroptosis in I/R injury, there is considerable interest in the potential role of ferroptosis as a targeted treatment for a wide range of I/R injury-related diseases. Recently, substantial progress has been made in applying ferroptosis to I/R injury in various organs and diseases. The development of ferroptosis regulators is expected to provide new opportunities for the treatment of I/R injury. Herein, we analytically review the pathological mechanism and targeted treatment of ferroptosis in I/R and related diseases from the perspectives of myocardial I/R injury, cerebral I/R injury, and ischemic renal injury.
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Kitade, Makoto, Hideaki Nakajima, Tetsuya Tsujikawa, Sakon Noriki, Tetsuya Mori, Yasushi Kiyono, Hidehiko Okazawa, and Akihiko Matsumine. "Evaluation of (R)-[11C]PK11195 PET/MRI for Spinal Cord-Related Neuropathic Pain in Patients with Cervical Spinal Disorders." Journal of Clinical Medicine 12, no. 1 (December 23, 2022): 116. http://dx.doi.org/10.3390/jcm12010116.
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Activated microglia are involved in secondary injury after acute spinal cord injury (SCI) and in development of spinal cord-related neuropathic pain (NeP). The aim of the study was to assess expression of translocator protein 18 kDa (TSPO) as an indicator of microglial activation and to investigate visualization of the dynamics of activated microglia in the injured spinal cord using PET imaging with (R)-[11C]PK11195, a specific ligand for TSPO. In SCI chimeric animal models, TSPO was expressed mainly in activated microglia. Accumulation of (R)-[3H]PK11195 was confirmed in autoradiography and its dynamics in the injured spinal cord were visualized by (R)-[11C]PK11195 PET imaging in the acute phase after SCI. In clinical application of (R)-[11C]PK11195 PET/MRI of the cervical spinal cord in patients with NeP related to cervical disorders, uptake was found in cases up to 10 months after injury or surgery. No uptake could be visualized in the injured spinal cord in patients with chronic NeP at more than 1 year after injury or surgery, regardless of the degree of NeP. However, a positive correlation was found between standardized uptake value ratio and the severity of NeP, suggesting the potential of clinical application for objective evaluation of chronic NeP.
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Son, Myeongjoo, Seyeon Oh, Chang Hu Choi, Kook Yang Park, Kuk Hui Son, and Kyunghee Byun. "Pyrogallol-Phloroglucinol-6,6-Bieckol from Ecklonia cava Attenuates Tubular Epithelial Cell (TCMK-1) Death in Hypoxia/Reoxygenation Injury." Marine Drugs 17, no. 11 (October 24, 2019): 602. http://dx.doi.org/10.3390/md17110602.
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The hypoxia/reoxygenation (H/R) injury causes serious complications after the blood supply to the kidney is stopped during surgery. The main mechanism of I/R injury is the release of high-mobility group protein B1 (HMGB1) from injured tubular epithelial cells (TEC, TCMK-1 cell), which triggers TLR4 or RAGE signaling, leading to cell death. We evaluated whether the extracts of Ecklonia cava (E. cava) would attenuate TEC death induced by H/R injury. We also evaluated which phlorotannin—dieckol (DK), phlorofucofuroeckol A (PFFA), pyrogallol phloroglucinol-6,6-bieckol (PPB), or 2,7-phloroglucinol-6,6-bieckol (PHB)—would have the most potent effect in the context of H/R injury. We used for pre-hypoxia treatment, in which the phlorotannins from E. cava extracts were added before the onset of hypoxia, and a post- hypoxia treatment, in which the phlorotannins were added before the start of reperfusion. PPB most effectively reduced HMGB1 release and the expression of TLR4 and RAGE induced by H/R injury in both pre- and post-hypoxia treatment. PPB also most effectively inhibited the expression of NF-kB and release of the inflammatory cytokines TNF-α and IL-6 in both models. PPB most effectively inhibited cell death and expression of cell death signaling molecules such as Erk/pErk, JNK/pJNK, and p38/pp38. These results suggest that PPB blocks the HGMB1–TLR4/RAGE signaling pathway and decreases TEC death induced by H/R and that PPB can be a novel target for renal H/R injury therapy.
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Arfian, Nur, Danny A. P. Wahyudi, Ingesti B. Zulfatina, Arsitya N. Citta, Nungki Anggorowati, Ali Multazam, Muhammad M. Romi, and Dwi C. R. Sari. "Chlorogenic Acid Attenuates Kidney Ischemic/Reperfusion Injury via Reducing Inflammation, Tubular Injury, and Myofibroblast Formation." BioMed Research International 2019 (September 22, 2019): 1–10. http://dx.doi.org/10.1155/2019/5423703.
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Kidney ischemic/reperfusion (I/R) injury is the main cause of acute kidney injury (AKI) involving renal function deterioration, renal architecture damage, and inflammation. This condition may lead to kidney fibrosis with epithelial to mesenchymal transition (EMT) and myofibroblast formation. Inhibition of chronic effects of kidney I/R injury may provide effective strategies for treating AKI and chronic kidney diseases (CKDs). Chlorogenic acid (CGA) is recognized as a powerful antioxidant, with anti-inflammatory and antifibrotic properties in many conditions. However, the effect of CGA on kidney I/R injury has not been elucidated yet. Kidney I/R injury was performed on male Swiss background mice (I/R group, n = 5, 3-4 months, 30–40 g) which underwent bilateral renal pedicles clamping for 30 minutes and then were euthanized on day three after operation. Three groups of I/R were treated with 3 different doses of CGA intraperitoneally for 2 days: 3.5 (I/R + CGA1 group), 7 (I/R + CGA2 group), and 14 (I/R + CGA3 group) mg/kg of body weight. Tubular injury was quantified based on Periodic Acid-Schiff staining, while reverse transcriptase PCR (RT-PCR) was performed to quantify mRNA expression of TGF-β1, vimentin, SOD-1, TLR-4, TNF-α, NF-κB and MCP-1. Immunohistochemical staining was done to quantify proliferating cell nuclear antigen (PCNA), myofibroblast (α-SMA), SOD-1 and macrophage (CD68) number. Kidney I/R demonstrated tubular injury and increased inflammatory mediator expression, macrophage number, and myofibroblast expansion. Meanwhile, histological analysis showed lower tubular injury with higher epithelial cell proliferation in CGA-treated groups compared to the I/R group. RT-PCR also revealed significantly lower TGF-β1 and vimentin mRNA expressions with higher SOD-1 mRNA expression. CGA-treated groups also demonstrated a significantly lower macrophage and myofibroblast number compared to the I/R group. These findings associated with lower mRNA expression of TLR-4, TNF-α, NF-κB, and MCP-1 as inflammatory mediators in CGA groups. I/R + CGA3 represented the highest amelioration effect among other CGA-treated groups. CGA treatment attenuates kidney I/R injury through reducing inflammation, decreasing myofibroblast expansion, and inducing epithelial cells proliferation.
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Tsukamoto, Takeshi, Bettina M. Buchholz, Asad Nazir, R. Savanh Chanthaphavong, Christopher Pape, Atsunori Nakao, and Anthony J. Bauer. "Molecular hydrogen prevents intestinal I/R injury." Journal of the American College of Surgeons 207, no. 3 (September 2008): S13. http://dx.doi.org/10.1016/j.jamcollsurg.2008.06.009.
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Kay, S. "Nerve injury." Current Orthopaedics 7, no. 4 (October 1993): 211–12. http://dx.doi.org/10.1016/0268-0890(93)90257-r.
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Torres, Alcy R. "Alcy R. Torres, MD." Revista Ecuatoriana de Pediatría 23, no. 4 (February 4, 2023): 1–38. http://dx.doi.org/10.52011/191.
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Dr Alcy Torres is a pediatric neurologist who specializes in traumatic brain injury. Much of his clinical work takes place around the Pediatric Concussion Program at Boston Medical Center; a multidisciplinary center coordinating care between the Emergency Room, the inpatient and outpatient services but also the common referrals to Physical, Vestibular, Ocular, Speech therapies and Neuropsychology services. His aim is to provide the highest level of care to children and adolescents who have sustained a brain injury by understanding the pathophysiology of the pediatric patient through research and enhancing the health and well-being of patients, minimizing distress, and preventing longer-term difficulties.In order to achieve this goal, he has developed a Standardized Clinical Assessment and Management Plans, now adopted by the Adult Concussion Clinic at Boston University to continuously review individual patient data for areas in our practice that need improvement, thus ensuring that the Brain Injury program always provides the best, most cost-effective care for our patients. Another goal of the center is access to acute and follow-up care, to which end we began developing an open access clinic in 2013 to provide services at Boston Medical Center, our satellites and across different different specialties.
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Zhao, Shanjun, and Lei Yu. "Sirtuin 1 activated by SRT1460 protects against myocardial ischemia/reperfusion injury." Clinical Hemorheology and Microcirculation 78, no. 3 (August 3, 2021): 271–81. http://dx.doi.org/10.3233/ch-201061.
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BACKGROUND: Ischemia reperfusion usually results in certain degree of damage to the myocardium, which is called myocardial ischemia/reperfusion (I/R) injury. OBJECTIVE: Previous studies have found that Sirt1 plays a critical role in I/R injury by protecting cardiac function. SRT1460 is the activator for Sirt1 that participates in the regulation of various diseases. However, whether SRT1460 has any effects on myocardial I/R injury needs further study. METHODS: The I/R rat model and H/R H9C2 model were established to simulate myocardial I/R injury. The infarct area of the rat heart was examined through TTC staining. The EF and FS of rats were detected through echocardiography. The levels of CK-MB, LDH, MDA, SOD and CK in cardiac tissues, serum or H9C2 cells were measured using commercial kits. Cell viability was assessed through MTT assay. Apoptosis was determined through flow cytometry analysis. Sirt1 expression was measured through western blot. RESULTS: Our work found that SRT1460 reduced the infarct area of the heart induced by myocardial I/R injury. In addition, SRT1460 was confirmed to ameliorate cardiac dysfunction induced by myocardial I/R injury. Further exploration discovered that SRT1460 weakened oxidative stress induced by myocardial I/R injury. Findings from in vitro assays demonstrated that SRT1460 relieved injury of H/R-treated H9C2 cells. Finally, rescue assays proved that Sirt1 knockdown reversed the protective effects of SRT1460 on the injury of H/R-treated H9C2 cells. CONCLUSION: Sirt1 activated by SRT1460 protected against myocardial I/R injury. This discovery may offer new sights on the treatment of myocardial I/R injury.
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Guo, Duo, Yan Chen, Dan Gao, and Xiuying Zhang. "CXC-chemokine receptor 4 antagonist prevents acute kidney injury potentially through recruiting bone marrow-derived stem cells." Journal of Biomedical Engineering and Informatics 2, no. 1 (December 3, 2015): 12. http://dx.doi.org/10.5430/jbei.v2n2p12.
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Background: Existing literature suggests that stromal-cell derived factor 1 (SDF-1) interacts with CXC-chemokine receptor 4 (CXCR4) in regulating the homing of stem cells derived from bone marrow. The CXCR4 antagonist, AMD3100, disrupts this SDF-1/CXCR4 interaction and triggers stem cell mobilization. We investigated whether AMD3100 could ameliorate renal ischemia reperfusion (I/R) injury via recruiting circulating stem cells to injured kidneys. Methods: We divided Sprague-Dawley rats into four groups, Sham, Sham + AMD3100, I/R, and I/R + AMD3100. All groups were treated with single subcutaneous injections of AMD3100 (5 mg/kg) or saline after sham surgery or I/R injury. Serum and renal tissues were harvested 12 hours and 3 days after treatment. We assessed survival, renal function changes, and histopathological alterations. TUNEL staining and caspase-3 expression levels were harnessed to measure tubular cell apoptosis, and circulating CXCR4 and CD34 positive mononuclear cells were identified by flow cytometry. Results: The I/R + AMD3100 group displayed significantly higher survival, lower serum creatinine, less prominent renal damage upon histopathological examination, and a lower degree of apoptosis than the I/R group. In addition, the AMD3100 treated group showed a significantly higher degree of CXCR4 and CD34 positive cell mobilization in the circulation and increased recruitment of these cells into the injured kidneys. Conclusions: AMD3100 promotes bone marrow stem cell mobilization and improves the recovery of renal function after I/R injury, and this effect may offer a promising therapeutic approach for acute kidney injury.
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Young, A. W. "Cotard delusion after brain injury." Neurocase 4, no. 3 (June 1, 1998): 255r—264. http://dx.doi.org/10.1093/neucas/4.3.255-r.
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Fu, Lin, Feng Ren, and Julien S. Baker. "Comparison of Joint Loading in Badminton Lunging between Professional and Amateur Badminton Players." Applied Bionics and Biomechanics 2017 (2017): 1–8. http://dx.doi.org/10.1155/2017/5397656.
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The knee and ankle are the two most injured joints associated with the sport of badminton. This study evaluates biomechanical factors between professional and amateur badminton players using an injury mechanism model. The aim of this study was to investigate the kinematic motion and kinetic loading differences of the right knee and ankle while performing a maximal right lunge. Amateur players exhibited greater ankle range of motion (p<0.05,r=0.89) and inversion joint moment (p<0.05,r=0.54) in the frontal plane as well as greater internal joint rotation moment (p<0.05,r=0.28) in the horizontal plane. In contrast, professional badminton players presented a greater knee joint moment in the sagittal (p<0.05,r=0.59) and frontal (p<0.05,r=0.37) planes, which may be associated with increased knee ligamentous injury risk. To avoid injury, the players need to forcefully extend the knee with internal rotation, strengthen the muscles around the ankle ligament, and maximise joint coordination during training. The injuries recorded and the forces responsible for the injuries seem to have developed during training activity. Training programmes and injury prevention strategies for badminton players should account for these findings to reduce potential injury to the ankle and knee.
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Xu, Yuerong, Wangang Guo, Di Zeng, Yexian Fang, Runze Wang, Dong Guo, Bingchao Qi, et al. "Inhibiting miR-205 Alleviates Cardiac Ischemia/Reperfusion Injury by Regulating Oxidative Stress, Mitochondrial Function, and Apoptosis." Oxidative Medicine and Cellular Longevity 2021 (June 29, 2021): 1–17. http://dx.doi.org/10.1155/2021/9986506.
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Background. miR-205 is important for oxidative stress, mitochondrial dysfunction, and apoptosis. The roles of miR-205 in cardiac ischemia/reperfusion (I/R) injury remain unknown. The aim of this research is to reveal whether miR-205 could regulate cardiac I/R injury by focusing upon the oxidative stress, mitochondrial function, and apoptosis. Methods. Levels of miR-205 and Rnd3 were examined in the hearts with I/R injury. Myocardial infarct size, cardiac function, oxidative stress, mitochondria function, and cardiomyocyte apoptosis were detected in mice with myocardial ischemia/reperfusion (MI/R) injury. The primary neonatal cardiomyocytes underwent hypoxia/reoxygenation (H/R) to simulate MI/R injury. Results. miR-205 levels were significantly elevated in cardiac tissues from I/R in comparison with those from Sham. In comparison with controls, levels of Rnd3 were significantly decreased in the hearts from mice with MI/R injury. Furthermore, inhibiting miR-205 alleviated MI/R-induced apoptosis, reduced infarct size, prevented oxidative stress increase and mitochondrial fragmentation, and improved mitochondrial functional capacity and cardiac function. Consistently, overexpression of miR-205 increased infarct size and promoted apoptosis, oxidative stress, and mitochondrial dysfunction in mice with MI/R injury. In cultured mouse neonatal cardiomyocytes, downregulation of miR-205 reduced oxidative stress in H/R-treated cardiomyocytes. Finally, inhibiting Rnd3 ablated the cardioprotective effects of miR-205 inhibitor in MI/R injury. Conclusions. We conclude that inhibiting miR-205 reduces infarct size, improves cardiac function, and suppresses oxidative stress, mitochondrial dysfunction, and apoptosis by promoting Rnd3 in MI/R injury. miR-205 inhibitor-induced Rnd3 activation is a valid target to treat MI/R injury.
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Xu, Dongwei, Jianjun Zhu, Seogsong Jeong, Dawei Li, Xiangwei Hua, Lifeng Huang, Jianjun Zhang, Yi Luo, and Qiang Xia. "Rictor Deficiency Aggravates Hepatic Ischemia/Reperfusion Injury in Mice by Suppressing Autophagy and Regulating MAPK Signaling." Cellular Physiology and Biochemistry 45, no. 6 (2018): 2199–212. http://dx.doi.org/10.1159/000488165.
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Background/Aims: The role of Rictor in hepatic ischemia/reperfusion (I/R) injury remains unknown. Here, we comprehensively examined the role of Rictor in hepatic I/R injury. Methods: We studied the expression of Rictor during hepatic I/R injury. The regulatory effects of Rictor on inflammatory responses, cytokine and chemokine release, apoptotic and anti-apoptotic responses, and autophagy induction during hepatic I/R injury were identified via the shRNA-mediated knockdown of Rictor. Subsequently, we collected the liver and blood samples of these mice to evaluate liver injury, mRNA and protein levels. Additionally, the signaling pathways induced by Rictor were investigated. Furthermore, the extent of activation of MAPKs in response to Rictor deficiency was investigated in lipopolysaccharide (LPS)-treated RAW264.7 cells. The mRNA expression levels were analyzed by real-time PCR, and the protein expression levels were analyzed using Western blot, immunofluorescence staining and enzyme-linked immunosorbent assay (ELISA). Results: The expression of Rictor was increased during hepatic I/R injury in vivo and hypoxia/reoxygenation (H/R) injury in vitro. Rictor deficiency enhanced the extent of liver injury by increasing macrophage and neutrophil infiltration, promoting cytokine and chemokine release, aggravating hepatocyte apoptosis, suppressing anti-apoptotic responses, and inhibiting autophagy induction during both hepatic I/R and H/R injury. Rictor was associated with the activation of hepatic I/R injury-induced MAPK signaling. In addition, Rictor deficiency affected MAPK activation in LPS-treated RAW264.7 cells. Conclusion: Rictor can substantially ameliorate I/R-induced liver injury. Therefore, our findings strongly suggest a therapeutic value of the Rictor/mTORC2 axis in hepatic I/R injury.
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Pan, Yihang, Xueke Wang, Xiwang Liu, Lihua Shen, Qixing Chen, and Qiang Shu. "Targeting Ferroptosis as a Promising Therapeutic Strategy for Ischemia-Reperfusion Injury." Antioxidants 11, no. 11 (November 6, 2022): 2196. http://dx.doi.org/10.3390/antiox11112196.
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Ischemia-reperfusion (I/R) injury is a major challenge in perioperative medicine that contributes to pathological damage in various conditions, including ischemic stroke, myocardial infarction, acute lung injury, liver transplantation, acute kidney injury and hemorrhagic shock. I/R damage is often irreversible, and current treatments for I/R injury are limited. Ferroptosis, a type of regulated cell death characterized by the iron-dependent accumulation of lipid hydroperoxides, has been implicated in multiple diseases, including I/R injury. Emerging evidence suggests that ferroptosis can serve as a therapeutic target to alleviate I/R injury, and pharmacological strategies targeting ferroptosis have been developed in I/R models. Here, we systematically summarize recent advances in research on ferroptosis in I/R injury and provide a comprehensive analysis of ferroptosis-regulated genes investigated in the context of I/R, as well as the therapeutic applications of ferroptosis regulators, to provide insights into developing therapeutic strategies for this devastating disease.
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Meyer, Luise J., and Matthias L. Riess. "Evaluation of In Vitro Neuronal Protection by Postconditioning with Poloxamer 188 Following Simulated Traumatic Brain Injury." Life 11, no. 4 (April 6, 2021): 316. http://dx.doi.org/10.3390/life11040316.
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Traumatic brain injury (TBI) leads to morbidity and mortality worldwide. Reperfusion after ischemia adds detrimental injury to cells. Ischemia/reperfusion (I/R) injures cells in a variety of ways including cell membrane disruption. Hence, methods to improve endogenous membrane resealing capacity are crucial. Poloxamer (P) 188, an amphiphilic triblock copolymer, was found to be effective against I/R and mechanical injury in various experimental settings. The aim of this study was to establish an in vitro mouse neuronal TBI model and, further, to investigate if postconditioning with P188 directly interacts with neurons after compression and simulated I/R injury, when administered at the start of reoxygenation. Cellular function was assessed by cell number/viability, mitochondrial viability, membrane damage by lactated dehydrogenase (LDH) release and FM1-43 incorporation as well as apoptosis-activation by Caspase 3. Five hours hypoxia ± compression with 2 h reoxygenation proved to be a suitable model for TBI. Compared to normoxic cells not exposed to compression, cell number and mitochondrial viability decreased, whereas membrane injury by LDH release/FM1-43 dye incorporation and Caspase 3 activity increased in cells exposed to hypoxic conditions with compression followed by reoxygenation. P188 did not protect neurons from simulated I/R and/or compression injury. Future research is indicated.
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Hu, Yulong, Zheng Wang, Nannan Ge, Ting Huang, Mingchao Zhang, and Hegui Wang. "Sodium pump alpha-2 subunit (ATP1A2) alleviates cardiomyocyte anoxia–reoxygenation injury via inhibition of endoplasmic reticulum stress-related apoptosis." Canadian Journal of Physiology and Pharmacology 96, no. 5 (May 2018): 515–20. http://dx.doi.org/10.1139/cjpp-2017-0349.
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Previous studies have found decreased functional capacity of the sodium pump (Na+-K+-ATPase) alpha and beta subunits and recovery of Na+-K+-ATPase activity significantly decreased myocyte apoptosis in myocardial ischemia–reperfusion (I/R) injury. However, the potential role of the Na+-K+-ATPase α-2 subunit (ATP1A2) in cardiomyocyte anoxia–reoxygenation (A/R) injury has not been elucidated. Rat myocardial cells were subjected to siRNA transfection followed by A/R injury. Apoptosis and expression of endoplasmic reticulum (ER) stress proteins CHOP, GRP78, and caspase-12 were detected in 4 groups of cells: ATP1A2 siRNA + A/R, control siRNA + A/R, control, and A/R injury model. We found that apoptosis was significantly elevated in the ATP1A2 siRNA + A/R group as compared with control siRNA + A/R, control, and A/R injury model groups (p < 0.05, p < 0.01, and p < 0.05). Furthermore, expression of CHOP, GRP78, and caspase-12 were significantly elevated in the ATP1A2 siRNA + A/R group as compared with control siRNA + A/R, control, and A/R injury model groups (p < 0.05, p < 0.01, and p < 0.05). Our findings suggest that cardiomyocyte ATP1A2 is a target of A/R injury, and its cardioprotective function may be mediated via inhibiting the ER-stress-related apoptosis.
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Zhou, Jiangqiao, Tao Qiu, Tianyu Wang, Zhongbao Chen, Xiaoxiong Ma, Long Zhang, and Jilin Zou. "USP4 deficiency exacerbates hepatic ischaemia/reperfusion injury via TAK1 signalling." Clinical Science 133, no. 2 (January 2019): 335–49. http://dx.doi.org/10.1042/cs20180959.
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Abstract Ubiquitin-specific peptidase 4 (USP4) protein is a type of deubiquitination enzyme that is correlated with many important biological processes. However, the function of USP4 in hepatic ischaemia/reperfusion (I/R) injury remains unknown. The aim of the present study was to explore the role of USP4 in hepatic I/R injury. USP4 gene knockout mice and primary hepatocytes were used to construct hepatic I/R models. The effect of USP4 on hepatic I/R injury was examined via pathological and molecular analyses. Our results indicated that USP4 was significantly up-regulated in liver of mice subjected to hepatic I/R injury. USP4 knockout mice exhibited exacerbated hepatic I/R injury, as evidenced by enhanced liver inflammation via the nuclear factor κB (NF-κB) signalling pathway and increased hepatocyte apoptosis. Additionally, USP4 overexpression inhibited hepatocyte inflammation and apoptosis on hepatic I/R stimulation. Mechanistically, our study demonstrates that USP4 deficiency exerts its detrimental effects on hepatic I/R injury by inducing activation of the transforming growth factor β-activated kinase 1 (TAK1)/JNK signalling pathways. TAK1 was required for USP4 function in hepatic I/R injury as TAK1 inhibition abolished USP4 function in vitro. In conclusion, our study demonstrates that USP4 deficiency plays a detrimental role in hepatic I/R injury by promoting activation of the TAK1/JNK signalling pathways. Modulation of this axis may be a novel strategy to alleviate the pathological process of hepatic I/R injury.
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Qiu, Tao, Tianyu Wang, Jiangqiao Zhou, Zhongbao Chen, Jilin Zou, Long Zhang, and Xiaoxiong Ma. "DUSP12 protects against hepatic ischemia–reperfusion injury dependent on ASK1-JNK/p38 pathway in vitro and in vivo." Clinical Science 134, no. 17 (September 2020): 2279–94. http://dx.doi.org/10.1042/cs20191272.
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Abstract Hepatic ischemia–reperfusion (I/R) injury is an important risk factor resulting in liver failure during liver surgery. However, there is still lack of effective therapeutic methods to treat hepatic I/R injury. DUSP12 is a member of the dual specific phosphatase (DUSP) family. Some DUSPs have been identified as being involved in the regulation of hepatic I/R injury. However, the role of DUSP12 during hepatic I/R injury is still unclear. In the present study, we observed a significant decrease in DUSP12 expression in a hepatic I/R injury mouse model in vivo and in hypoxia/reoxygenation (H/R) model in vitro. Using hepatocyte-specific DUSP12 knockout mice and DUSP12 transgenic mice, we demonstrated that DUSP12 apparently relieved I/R-induced liver injury. Moreover, DUSP12 inhibited hepatic inflammatory responses and alleviated apoptosis both in vitro and in vivo. Furthermore, we demonstrated that JNK and p38 activity, but not ERK1/2, was increased in the DUSP12-deficient mice and decreased in the DUSP12 transgenic mice under I/R condition. ASK1 was required for DUSP12 function in hepatic I/R injury and inhibition of ASK1 prevented inflammation and apoptosis in DUSP12-deficient hepatocytes and mice. In conclusion, DUSP12 protects against hepatic I/R injury and related inflammation and apoptosis. This regulatory role of DUSP12 is primarily through ASK1-JNK/p38 signaling pathway. Taken together, DUSP12 could be a potential therapeutic target for hepatic I/R injury.
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Zhang, Yamin, Xiaoying Fan, and Hua Yang. "Long noncoding RNA FTX ameliorates hydrogen peroxide-induced cardiomyocyte injury by regulating the miR-150/KLF13 axis." Open Life Sciences 15, no. 1 (December 31, 2020): 1000–1012. http://dx.doi.org/10.1515/biol-2020-0100.
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AbstractBackgroundMyocardial reperfusion is an effective therapy for acute myocardial infarction (AMI). However, ischemia/reperfusion (I/R) injury following myocardial reperfusion is a significant limitation for AMI treatment. Five prime to Xist (FTX) was recognized as a biomarker of multiple diseases, including heart disease. However, the molecular mechanism of FTX in I/R injury is unclear.MethodsCell viability was evaluated by using cell counting kit-8 (CCK-8) assay. Apoptosis was analyzed by using a caspase-3 activity detection kit and flow cytometry. The expression of FTX, microRNA (miR)-150, and Kruppel-like factor 13 (KLF13) was measured by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The interaction of miR-150 and FTX or KLF13 was confirmed by a dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Protein expression of KLF13 was examined by Western blot. The role of FTX was detected in I/R-injured heart tissues in vivo.ResultsHydrogen peroxide (H2O2) induced cardiomyocyte injury by decreasing cell viability and expediting cell apoptosis. However, FTX alleviated cardiomyocyte injury by promoting cell proliferation and restricting cell apoptosis of H9C2 cells that were treated with H2O2. In addition, we discovered that FTX directly interacted with miR-150, while KLF13 was a target of miR-150. Rescue experiments showed that miR-150 neutralized the FTX-mediated promotion of cell progression and restriction of cell apoptosis in H9C2 cells treated with H2O2. KLF13 knockdown restored the effect of miR-150 on increased proliferation and decrease in apoptosis in H2O2-treated cardiomyocytes. Furthermore, FTX enhanced the expression of KLF13 protein through interaction with miR-150. Upregulation of FTX repressed apoptosis in I/R-injured heart tissues in vivo.ConclusionFTX relieves H2O2-induced cardiomyocyte injury by increasing KLF13 expression via depletion of miR-150, thus providing a novel therapeutic target for the alleviation of I/R injury.
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Pille, Johannes A., and Matthias L. Riess. "Potential Effects of Poloxamer 188 on Rat Isolated Brain Mitochondria after Oxidative Stress In Vivo and In Vitro." Brain Sciences 11, no. 1 (January 18, 2021): 122. http://dx.doi.org/10.3390/brainsci11010122.
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Outcome after cerebral ischemia is often dismal. Reperfusion adds significantly to the ischemic injury itself. Therefore, new strategies targeting ischemia/reperfusion (I/R) injury are critically needed. Poloxamer (P)188, an amphiphilic triblock copolymer, is a highly promising pharmacological therapeutic as its capability to insert into injured cell membranes has been reported to protect against I/R injury in various models. Although mitochondrial function particularly profits from P188 treatment after I/R, it remains unclear if this beneficial effect occurs directly or indirectly. Here, rat isolated brain mitochondria underwent oxidative stress in vivo by asphyxial cardiac arrest or in vitro by the addition of hydrogen peroxide (H2O2) after isolation. Mitochondrial function was assessed by adenosine triphosphate synthesis, oxygen consumption, and calcium retention capacity. Both asphyxia and H2O2 exposure significantly impaired mitochondrial function. P188 did not preserve mitochondrial function after either injury mechanism. Further research is indicated.
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Brock, Robert W., Michael W. Carson, Kenneth A. Harris, and Richard F. Potter. "Microcirculatory perfusion deficits are not essential for remote parenchymal injury within the liver." American Journal of Physiology-Gastrointestinal and Liver Physiology 277, no. 1 (July 1, 1999): G55—G60. http://dx.doi.org/10.1152/ajpgi.1999.277.1.g55.
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A normotensive model of hindlimb ischemia-reperfusion in Wistar rats was used to test the hypothesis that microvascular perfusion deficits contribute to the initiation of remote hepatic injury during a systemic inflammatory response. Animals were randomly assigned to one of three groups: 4 h of ischemia with 6 h of reperfusion (I/R-6; n = 4), 4 h of ischemia with 3 h of reperfusion (I/R-3; n = 5), or no ischemia (naive; n = 5). With intravital fluorescence microscopy, propidium iodide (PI; 0.05 mg/100 g body wt) was injected for the in vivo labeling of lethally injured hepatocytes (number/10−1mm3). PI-positive hepatocytes increased progressively over the 6-h period (naive 32.9 ± 7.8 vs. I/R-3 92.8 ± 11.5 vs. I/R-6 232 ± 39.2), with no difference between periportal and pericentral regions of the lobule. Additionally, a significant decrease in continuously perfused sinusoids (naive 70.0 ± 1.5 vs. I/R-3 65.0 ± 1.0 vs. I/R-6 48.8 ± 0.9%) was measured. Regional sinusoidal perfusion differences were only observed after 3 h of limb reperfusion. Indirect measures of hepatocellular injury using alanine transaminase levels support the progressive nature of hepatic parenchymal injury (0 h 57.8 ± 6.5 vs. 3 h 115.3 ± 20.7 vs. 6 h 125.6 ± 19.5 U/l). Evidence from this study suggests that remote hepatic parenchymal injury occurs early and progresses after the induction of a systemic inflammatory response and that microvascular perfusion deficits are not essential for the initiation of such injury.
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Michinaga, Shotaro, Shigeru Hishinuma, and Yutaka Koyama. "Roles of Astrocytic Endothelin ETB Receptor in Traumatic Brain Injury." Cells 12, no. 5 (February 24, 2023): 719. http://dx.doi.org/10.3390/cells12050719.
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Traumatic brain injury (TBI) is an intracranial injury caused by accidents, falls, or sports. The production of endothelins (ETs) is increased in the injured brain. ET receptors are classified into distinct types, including ETA receptor (ETA-R) and ETB receptor (ETB-R). ETB-R is highly expressed in reactive astrocytes and upregulated by TBI. Activation of astrocytic ETB-R promotes conversion to reactive astrocytes and the production of astrocyte-derived bioactive factors, including vascular permeability regulators and cytokines, which cause blood–brain barrier (BBB) disruption, brain edema, and neuroinflammation in the acute phase of TBI. ETB-R antagonists alleviate BBB disruption and brain edema in animal models of TBI. The activation of astrocytic ETB receptors also enhances the production of various neurotrophic factors. These astrocyte-derived neurotrophic factors promote the repair of the damaged nervous system in the recovery phase of patients with TBI. Thus, astrocytic ETB-R is expected to be a promising drug target for TBI in both the acute and recovery phases. This article reviews recent observations on the role of astrocytic ETB receptors in TBI.
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Wen, Cong, Meide Lan, Xin Tan, Xiaobo Wang, Zaiyong Zheng, Mingming Lv, Xuemei Zhao, et al. "GSK3β Exacerbates Myocardial Ischemia/Reperfusion Injury by Inhibiting Myc." Oxidative Medicine and Cellular Longevity 2022 (April 29, 2022): 1–23. http://dx.doi.org/10.1155/2022/2588891.
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Myocardial ischemia/reperfusion (MI/R) injury is a life-threatening disease with high morbidity and mortality. Herein, the present study is conducted to explore the regulatory mechanism of GSK3β in MI/R injury regarding cardiomyocyte apoptosis and oxidative stress. The MI/R injury mouse model and hypoxic reoxygenation (H/R) cell model were established. The expression pattern of GSK3β, FTO, KLF5, and Myc was determined followed by their relation validation. Next, loss-of-function experiments were implemented to verify the effect of GSK3β/FTO/KLF5/Myc on cardiomyocyte apoptosis and oxidative stress in the MI/R injury mouse model and H/R cell model. High expression of GSK3β and low expression of FTO, KLF5, and Myc were observed in the MI/R injury mouse model and H/R cell model. GSK3β promoted phosphorylation of FTO and KLF5, thus increasing the ubiquitination degradation of FTO and KLF5. A decrease of FTO and KLF5 was able to downregulate Myc expression, resulting in enhanced cardiomyocyte apoptosis and oxidative stress. These data together supported the crucial role that GSK3β played in facilitating cardiomyocyte apoptosis and oxidative stress so as to accelerate MI/R injury, which highlights a promising therapeutic strategy against MI/R injury.
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Ma, Sai, Zhengxun Zhang, Fu Yi, Yabin Wang, Xiaotian Zhang, Xiujuan Li, Yuan Yuan, and Feng Cao. "Protective Effects of Low-Frequency Magnetic Fields on Cardiomyocytes from Ischemia Reperfusion InjuryviaROS and NO/ONOO−." Oxidative Medicine and Cellular Longevity 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/529173.
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Background. Cardiac ischemia reperfusion (I/R) injury is associated with overproduction of reactive oxygen species (ROS). Low frequency pulse magnetic fields (LFMFs) have been reported to decrease ROS generation in endothelial cells. Whether LFMFs could assert protective effects on myocardial from I/R injuryviaROS regulation remains unclear.Methods. To simulatein vivocardiac I/R injury, neonatal rat cardiomyocytes were subjected to hypoxia reoxygenation (H/R) with or without exposure to LFMFs. Cell viability, apoptosis index, ROS generation (includingO2-and ONOO−), and NO production were measured in control, H/R, and H/R + LFMF groups, respectively.Results. H/R injury resulted in cardiomyocytes apoptosis and decreased cell viability, whereas exposure to LFMFs before or after H/R injury significantly inhibited apoptosis and improved cell viability (P<0.05). LFMFs treatment could suppress ROS (includingO2-and ONOO−) generation induced by H/R injury, combined with decreased NADPH oxidase activity. In addition, LFMFs elevated NO production and enhanced NO/ONOO−balance in cardiomyocytes, and this protective effect wasviathe phosphorylation of endothelial nitric oxide synthase (eNOS).Conclusion. LFMFs could protect myocardium against I/R injuryviaregulating ROS generation and NO/ONOO−balance. LFMFs treatment might serve as a promising strategy for cardiac I/R injury.
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Ali Sheikh, Md Sayed. "Overexpression of miR-375 Protects Cardiomyocyte Injury following Hypoxic-Reoxygenation Injury." Oxidative Medicine and Cellular Longevity 2020 (January 3, 2020): 1–10. http://dx.doi.org/10.1155/2020/7164069.
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The aim of the study was to evaluate the clinical significance of microRNA-375 in acute myocardial infarction patients and its mimic action in hypoxia/reoxygenation- (H/R-) induced ventricular cardiomyocyte H9c2 injury. In the current study, 90 ST-elevated acute MI patients (STEMI), 75 non-ST-elevated acute MI patients (NSTEMI), 90 healthy subjects, 14 weeks old mice, and ventricular cardiomyocyte H9c2 were included. The expressions of plasma microRNA-375 in patients with STEMI and NSTEMI and AMI mouse models were remarkably decreased than in controls (P<0.001). The areas under the curve (AUC) of plasma microRNA-375 were revealed 0.939 in STEMI and 0.935 in NSTEMI subjects. Moreover, microRNA-375 levels in H/R-exposed cardiac H9c2 cells were evidently downregulated and significantly increased apoptosis rate and caspase-3 activity levels, while overexpression of miR-375 remarkably reduced apoptosis percentage and caspase-3 levels as compared with normal cells. Furthermore, this study also demonstrated that Nemo-like kinase (NLK), NLK mRNA, and protein expression levels were significantly downregulated in H/R-injured H9c2 cells, on the contrary, H9c2 cells transfected with mimic-miR-375 greatly upregulated NLK mRNA and protein expression. Plasma microRNA-375 may serve as an essential clinical biomarker for diagnosis of early-stage AMI. Mimic expression of miR-375 significantly prevented H/R-induced cardiomyocyte injury by decreasing caspase-3 activity through upregulation of the NLK gene, recommended as a new therapeutic option for AMI patient.
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Arfian, Nur, Dwi C. Ratna Sari, Muhammad M. Romi, Dian P. Wibisono, and Noriaki Emoto. "HEPARANASE EXPRESSION IN RENAL INTERSTITIAL MAY CONTRIBUTE TO EPITHELIAL AND ENDOTHELIAL CELLS INJURIES AFTER KIDNEY ISCHEMIC/ REPERFUSION EPISODE IN MICE." KnE Life Sciences 2, no. 1 (September 20, 2015): 70. http://dx.doi.org/10.18502/kls.v2i1.119.
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Kidney ischemia/reperfusion injury (I/R) is the most frequent cause of acute kidney injury (AKI). It had been reported that epithelial and endothelial injuries occurred during kidney I/R injury. Heparanase is an enzyme that degrades glycocalyx and contributes to I/R injury in the heart and liver. This study is to elucidate the association between heparanase expression and cell injuries in kidney I/R injury. We performed kidney I/R injury model in mice using renal pedicle clamping for 30 minutes and sacrificed the mice in day 1 (n=6) after operation. Sham-operation procedure (SO, n=5) was used as control. PAS staining was used to quantify tubular injury score. Serum creatinine was measured from orbital venous. Heparanase expression was quantified using western blot and real-time PCR. Heparanase localization and endothelial injury were shown by immunostaining of heparanase and double glycocalyx-von Willebrand factor. Kidney I/R induced an increase of serum creatinine level that was accompanied by elevation of tubular injury score and glycocalyx damage. Glycocalyx damage was identified using immunofluorescent staining that revealed a disruption of glycocalyx or lectin layer in the endothelial cells of intra-renal artery. This finding was associated with significant elevation of heparanase mRNA and protein level expression. We found that heparanase was expressed in the renal epithelial and interstitial cells. In conclusion, heparanase may induce endothelial and epithelial injury in the kidney I/R episode. Using heparanase expression as a early marker of AKI may possibly promising. Keywords: kidney I/R, epithelial injury, endothelial injury, heparanase, glycocalyx
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He, Yanjing, Yin Cai, Tianhao Sun, Liangqing Zhang, Michael G. Irwin, Aimin Xu, and Zhengyuan Xia. "MicroRNA-503 Exacerbates Myocardial Ischemia/Reperfusion Injury via Inhibiting PI3K/Akt- and STAT3-Dependent Prosurvival Signaling Pathways." Oxidative Medicine and Cellular Longevity 2022 (May 17, 2022): 1–17. http://dx.doi.org/10.1155/2022/3449739.
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Acute myocardial infarction is a leading cause of death worldwide, while restoration of blood flow to previously ischemic myocardium may lead to ischemia/reperfusion (I/R) injury. Accumulated evidence shows that microRNAs play important roles in cardiovascular diseases. However, the potential role of microRNA-503 (miR-503) in myocardial I/R injury is little known. Thus, this study is aimed at determining whether and how miR-503 affects myocardial I/R injury in vivo and in vitro. A mouse model of myocardial I/R injury and H9c2 cell model of hypoxia/reoxygenation (H/R) injury were established. The postischemic cardiac miR-503 was downregulated in vivo and in vitro. Mechanistically, PI3K p85 and Bcl-2 are miR-503 targets. The post-ischemic cardiac PI3K p85 protein level was decreased in vivo. Agomir-503 treatment exacerbated H/R-induced injuries manifested as decreased cell viability, increased lactate dehydrogenase activity, and cell apoptosis. Agomir-503 treatment reduced cell viability under normoxia as well and reduced both PI3K p85 and Bcl-2 protein levels under either normoxia or H/R condition. It reduced phosphorylation of Stat3 (p-Stat3-Y705) and Akt (T450) in cells subjected to H/R. In contrast, Antagomir-503 treatment attenuated H/R injury and increased p-Stat3 (Y705) under normoxia and increased p-Akt (T450) under either normoxia or H/R condition. It is concluded that miR-503 exacerbated I/R injury via inactivation of PI3K/Akt and STAT3 pathways and may become a therapeutic target in preventing myocardial I/R injury.
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Lin, Fengxia, Luhua Xu, Meizhu Huang, Bin Deng, Weiwei Zhang, Zhicong Zeng, and Song Yinzhi. "β-Sitosterol Protects against Myocardial Ischemia/Reperfusion Injury via Targeting PPARγ/NF-κB Signalling." Evidence-Based Complementary and Alternative Medicine 2020 (March 28, 2020): 1–9. http://dx.doi.org/10.1155/2020/2679409.
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Myocardial ischemia/reperfusion (I/R) injury is a clinically severe complication, which can cause high rates of disability and mortality particularly in patients with myocardial infarction, yet the molecular mechanisms underlying this process remain unclear. This study aimed to explore the protective effects of β-sitosterol against myocardial I/R injury and to elucidate the underlying molecular mechanisms. Our results showed that hypoxia/reoxygenation (H/R) treatment suppressed cell viability, induced cell apoptosis and reactive oxygen species production, increased caspase-3 and -9 activities, upregulated caspase-3 and -9 protein expressions, downregulated the Bcl-2 protein expression, and reduced the mitochondrial membrane potential. β-Sitosterol treatment attenuated H/R-induced cardiomyocyte injury. Moreover, β-sitosterol treatment counteracted the inhibitory effects of H/R treatment on the peroxisome proliferator-activated receptor gamma (PPARγ) expression and enhanced effects of H/R treatment on the NF-κB expression in cardiomyocytes. Furthermore, inhibition of PPARγ impaired the protective actions of β-sitosterol against H/R-induced cardiomyocyte injury. In the I/R rats, β-sitosterol treatment reduced the myocardial infarcted size and apoptosis, which was attenuated by the inhibition of PPARγ. In conclusion, our results demonstrate that β-sitosterol protected against in vitro H/R-induced cardiomyocyte injury and in vivo myocardial I/R injury. The β-sitosterol-mediated cardioprotective effects may involve the modulation of PPARγ/NF-κB signalling during myocardial I/R injury. Further studies are required to further explore the clinical application of β-sitosterol in the myocardial I/R injury.
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Surinkaew, Poomarin, Nattayaporn Apaijai, Passakorn Sawaddiruk, Thidarat Jaiwongkam, Sasiwan Kerdphoo, Nipon Chattipakorn, and Siriporn C. Chattipakorn. "Mitochondrial Fusion Promoter Alleviates Brain Damage in Rats with Cardiac Ischemia/Reperfusion Injury." Journal of Alzheimer's Disease 77, no. 3 (September 29, 2020): 993–1003. http://dx.doi.org/10.3233/jad-200495.
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Background: Cardiac ischemia/reperfusion (I/R) injury induces brain damage through increased blood-brain barrier (BBB) breakdown, microglial hyperactivity, pro-inflammatory cytokines, amyloid-β deposition, loss of dendritic spines, brain mitochondrial dysfunction, and imbalanced mitochondrial dynamics. Previous studies demonstrated that mitochondrial fusion promoter reduced cardiac damage from cardiac I/R injury; however, following cardiac I/R injury, the roles of mitochondrial dynamics on the brain have not been investigated. Objective: To investigate the effects of pharmacological modulation using mitochondrial fusion promoter (M1) in the brain of rats following cardiac I/R injury. Methods: Twenty-four male Wistar rats were separated into two groups; 1) sham-operation (n = 8) and 2) cardiac I/R injury (n = 16). Rats in the cardiac I/R injury group were randomly received either normal saline solution as a vehicle or a mitochondrial fusion promoter (M1, 2 mg/kg) intravenously. Both treatments were given to the rats 15 minutes before cardiac I/R injury. At the end of the reperfusion protocol, the brain was rapidly removed to investigate brain mitochondrial function, mitochondrial dynamics proteins, microglial activity, and Alzheimer’s disease (AD) related proteins. Results: Cardiac I/R injury induced brain mitochondrial dynamics imbalance as indicated by reduced mitochondrial fusion proteins expression without alteration in mitochondrial fission, brain mitochondrial dysfunction, BBB breakdown, increased macrophage infiltration, apoptosis, and AD-related proteins. Pretreatment with M1 effectively increased the expression of mitofusin 2, a mitochondrial outer membrane fusion protein, reduced brain mitochondrial dysfunction, BBB breakdown, macrophage infiltration, apoptosis, and AD-related proteins in rats following cardiac I/R injury. Conclusion: This mitochondrial fusion promoter significantly protected rats with cardiac I/R injury against brain damage.
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Ye, Chunlin, Wanghong Qi, Shaohua Dai, Guowen Zou, Weicheng Liu, Bentong Yu, and Jian Tang. "microRNA-223 promotes autophagy to aggravate lung ischemia-reperfusion injury by inhibiting the expression of transcription factor HIF2α." American Journal of Physiology-Lung Cellular and Molecular Physiology 319, no. 1 (July 1, 2020): L1—L10. http://dx.doi.org/10.1152/ajplung.00009.2020.
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Lung ischemia-reperfusion (I/R) injury severely endangers human health, and recent studies have suggested that certain microRNAs (miRNAs) play important roles in this pathological phenomenon. The current study aimed to ascertain the ability of miR-223 to influence lung I/R injury by targeting hypoxia-inducible factor-2α (HIF2α). First, mouse models of lung I/R injury were established: during surgical procedures, pulmonary arteries and veins and unilateral pulmonary portal vessels were blocked and resuming bilateral pulmonary ventilation, followed by restoration of bipulmonary ventilation. In addition, a lung I/R injury cell model was constructed by exposure to hypoxic reoxygenation (H/R) in mouse pulmonary microvascular endothelial cells (PMVECs). Expression of miR-223, HIF2α, and β-catenin in tissues or cells was determined by RT-qPCR and Western blot analysis. Correlation between miR-223 and HIF2α was analyzed by dual luciferase reporter gene assay. Furthermore, lung tissue injury and mouse PMVEC apoptosis was evaluated by hematoxylin and eosin (H&E), TUNEL staining, and flow cytometry. Autophagosomes in cells were detected by light chain 3 immunofluorescence assay. miR-223 was expressed at a high level while HIF2α/β-catenin was downregulated in tissues and cells with lung I/R injury. Furthermore, miR-223 targeted and repressed HIF2α expression to downregulate β-catenin expression. The miR-223/HIF2α/β-catenin axis aggravated H/R injury in mouse PMVECs and lung I/R injury in mice by enhancing autophagy. Taken together, miR-223 inhibits HIF2α to repress β-catenin, thus contributing to autophagy to complicate lung I/R injury. These findings provide a promising therapeutic target for treating lung I/R injury.
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Yang, Mu, Jian-Xin Dong, Lu-Bin Li, Hai-Jie Che, Jun Yong, Fu-Bo Song, Tao Wang, and Jv-Wen Zhang. "Local and Remote Postconditioning Decrease Intestinal Injury in a Rabbit Ischemia/Reperfusion Model." Gastroenterology Research and Practice 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/2604032.
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Intestinal ischemia/reperfusion (I/R) injury is a significant problem that is associated with high morbidity and mortality in critical settings. This injury may be ameliorated using postconditioning protocol. In our study, we created a rabbit intestinal I/R injury model to analyze the effects of local ischemia postconditioning (LIPo) and remote ischemia postconditioning (RIPo) on intestinal I/R injury. We concluded that LIPo affords protection in intestinal I/R injury in a comparable fashion with RIPo by decreasing oxidative stress, neutrophil activation, and apoptosis.
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Lee, H. Thomas, Mihwa Kim, Joo Yun Kim, Kevin M. Brown, Ahrom Ham, Vivette D. D'Agati, and Yuko Mori-Akiyama. "Critical role of interleukin-17A in murine intestinal ischemia-reperfusion injury." American Journal of Physiology-Gastrointestinal and Liver Physiology 304, no. 1 (January 1, 2013): G12—G25. http://dx.doi.org/10.1152/ajpgi.00201.2012.
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Intestinal ischemia-reperfusion (I/R) injury causes severe illness frequently complicated by remote multiorgan dysfunction and sepsis. Recent studies implicated interleukin-17A (IL-17A) in regulating inflammation, autoimmunity, and I/R injury. Here, we determined whether IL-17A is critical for generation of intestinal I/R injury and subsequent liver and kidney injury. Mice subjected to 30 min of superior mesenteric artery ischemia not only developed severe small intestinal injury (necrosis, apoptosis, and neutrophil infiltration) but also developed significant renal and hepatic injury. We detected large increases in IL-17A in the small intestine, liver, and plasma. IL-17A is critical for generating these injuries, since genetic deletion of IL-17A- or IL-17A-neutralizing antibody treatment markedly protected against intestinal I/R injury and subsequent liver and kidney dysfunction. Intestinal I/R caused greater increases in portal plasma and small intestine IL-17A, suggesting an intestinal source for IL-17A generation. We also observed that intestinal I/R caused rapid small intestinal Paneth cell degranulation and induced murine α-defensin cryptdin-1 expression. Furthermore, genetic or pharmacological depletion of Paneth cells significantly attenuated the intestinal I/R injury as well as hepatic and renal dysfunction. Finally, Paneth cell depletion significantly decreased small intestinal, hepatic, and plasma IL-17A levels after intestinal I/R. Taken together, we propose that Paneth cell-derived IL-17A may play a critical role in intestinal I/R injury as well as extraintestinal organ dysfunction.