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Journal articles on the topic 'Liver Ischemia Repercussion Injury'

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Author: Grafiati

Published: 14 March 2023

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1

Cursio, Raffaele, Pascal Colosetti, and Jean Gugenheim. "Autophagy and Liver Ischemia-Reperfusion Injury." BioMed Research International 2015 (2015): 1–16. http://dx.doi.org/10.1155/2015/417590.

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Liver ischemia-reperfusion (I-R) injury occurs during liver resection, liver transplantation, and hemorrhagic shock. The main mode of liver cell death after warm and/or cold liver I-R is necrosis, but other modes of cell death, as apoptosis and autophagy, are also involved. Autophagy is an intracellular self-digesting pathway responsible for removal of long-lived proteins, damaged organelles, and malformed proteins during biosynthesis by lysosomes. Autophagy is found in normal and diseased liver. Although depending on the type of ischemia, warm and/or cold, the dynamic process of liver I-R results mainly in adenosine triphosphate depletion and in production of reactive oxygen species (ROS), leads to both, a local ischemic insult and an acute inflammatory-mediated reperfusion injury, and results finally in cell death. This process can induce liver dysfunction and can increase patient morbidity and mortality after liver surgery and hemorrhagic shock. Whether autophagy protects from or promotes liver injury following warm and/or cold I-R remains to be elucidated. The present review aims to summarize the current knowledge in liver I-R injury focusing on both the beneficial and the detrimental effects of liver autophagy following warm and/or cold liver I-R.

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2

Saidi, Rezà F., and Seyed Kamran Hejazi Kenari. "Liver Ischemia/Reperfusion Injury: an Overview." Journal of Investigative Surgery 27, no. 6 (July 24, 2014): 366–79. http://dx.doi.org/10.3109/08941939.2014.932473.

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3

Ildefonso, José Ángel, and Javier Arias-Díaz. "Pathophysiology of liver ischemia—Reperfusion injury." Cirugía Española (English Edition) 87, no. 4 (January 2010): 202–9. http://dx.doi.org/10.1016/s2173-5077(10)70049-1.

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4

Shibayama, Yuro, Shosaku Asaka, and Akira Nishijima. "Mechanism of liver injury following ischemia." Experimental and Molecular Pathology 55, no. 3 (December 1991): 251–60. http://dx.doi.org/10.1016/0014-4800(91)90005-i.

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5

Ai-Min, H. "Liver injury following normothermic ischemia in steatotic rat liver." Hepatology 20, no. 5 (November 1994): 1287–93. http://dx.doi.org/10.1016/0270-9139(94)90770-6.

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6

Hui, Ai-Min, Seiji Kawasaki, Masatoshi Makuuchi, Jun Nakayama, Toshihiko Ikegami, and Shinichi Miyagawa. "Liver injury following normothermic ischemia in steatotic rat liver." Hepatology 20, no. 5 (November 1994): 1287–93. http://dx.doi.org/10.1002/hep.1840200528.

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7

Wang, Hai, Zhifeng Xi, Lu Deng, Yixiao Pan, Kang He, and Qiang Xia. "Macrophage Polarization and Liver Ischemia-Reperfusion Injury." International Journal of Medical Sciences 18, no. 5 (2021): 1104–13. http://dx.doi.org/10.7150/ijms.52691.

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8

Wang, Hai, Zhifeng Xi, Lu Deng, Yixiao Pan, Kang He, and Qiang Xia. "Macrophage Polarization and Liver Ischemia-Reperfusion Injury." International Journal of Medical Sciences 18, no. 5 (2021): 1104–13. http://dx.doi.org/10.7150/ijms.52691.

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9

de Rougemont, Olivier, Philipp Dutkowski, and Pierre-Alain Clavien. "Biological modulation of liver ischemia–reperfusion injury." Current Opinion in Organ Transplantation 15, no. 2 (April 2010): 183–89. http://dx.doi.org/10.1097/mot.0b013e3283373ced.

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10

Jones, Ryan T., Luis H. Toledo-Pereyra, and Kelly M. Quesnelle. "Selectins in Liver Ischemia and Reperfusion Injury." Journal of Investigative Surgery 28, no. 5 (September 3, 2015): 292–300. http://dx.doi.org/10.3109/08941939.2015.1056920.

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11

Imamura, Hiroshi, Michel Dagenais, Lise Giroux, Antoine Brault, and P.-Michel Huet. "COLD ISCHEMIA-REPERFUSION INJURY OF THE LIVER." Transplantation 60, no. 1 (July 1995): 14–19. http://dx.doi.org/10.1097/00007890-199507150-00003.

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12

Kupiec-Weglinski, J. W., and R. W. Busuttil. "Ischemia and Reperfusion Injury in Liver Transplantation." Transplantation Proceedings 37, no. 4 (May 2005): 1653–56. http://dx.doi.org/10.1016/j.transproceed.2005.03.134.

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13

Selzner, Markus, Hannes Andreas Rudiger, David Sindram, and Pierre-Alain Clavien. "Ischemia/reperfusion injury in the steatotic liver." Gastroenterology 118, no. 4 (April 2000): A1002. http://dx.doi.org/10.1016/s0016-5085(00)86160-0.

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14

Teixeira, Roberto, Nilza Molan, Marcia S. Kubrusly, Marta Privato, Ana Maria M. Coelho, Telesforo Bacchella, and Marcel C. Machado. "T1910 Postconditioning in Liver Ischemia-Reperfusion Injury." Gastroenterology 134, no. 4 (April 2008): A—893. http://dx.doi.org/10.1016/s0016-5085(08)64195-5.

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15

Nastos, Constantinos, Konstantinos Kalimeris, Nikolaos Papoutsidakis, Marios-Konstantinos Tasoulis, Panagis M. Lykoudis, Kassiani Theodoraki, Despoina Nastou, Vassilios Smyrniotis, and Nikolaos Arkadopoulos. "Global Consequences of Liver Ischemia/Reperfusion Injury." Oxidative Medicine and Cellular Longevity 2014 (2014): 1–13. http://dx.doi.org/10.1155/2014/906965.

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Liver ischemia/reperfusion injury has been extensively studied during the last decades and has been implicated in the pathophysiology of many clinical entities following hepatic surgery and transplantation. Apart from its pivotal role in the pathogenesis of the organ’s post reperfusion injury, it has also been proposed as an underlying mechanism responsible for the dysfunction and injury of other organs as well. It seems that liver ischemia and reperfusion represent an event with “global” consequences that influence the function of many remote organs including the lung, kidney, intestine, pancreas, adrenals, and myocardium among others. The molecular and clinical manifestation of these remote organs injury may lead to the multiple organ dysfunction syndrome, frequently encountered in these patients. Remote organ injury seems to be in part the result of the oxidative burst and the inflammatory response following reperfusion. The present paper aims to review the existing literature regarding the proposed mechanisms of remote organ injury after liver ischemia and reperfusion.

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16

Zaki, Hala Fahmy, and Rania Mohsen Abdelsalam. "Vinpocetine protects liver against ischemia–reperfusion injury." Canadian Journal of Physiology and Pharmacology 91, no. 12 (December 2013): 1064–70. http://dx.doi.org/10.1139/cjpp-2013-0097.

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Hepatic ischemia–reperfusion (IR) injury is a clinical problem that leads to cellular damage and organ dysfunction mediated mainly via production of reactive oxygen species and inflammatory cytokines. Vinpocetine has long been used in cerebrovascular disorders. This study aimed to explore the protective effect of vinpocetine in IR injury to the liver. Ischemia was induced in rats by clamping the common hepatic artery and portal vein for 30 min followed by 30 min of reperfusion. Serum transaminases and liver lactate dehydrogenase (LDH) activities, liver inflammatory cytokines, oxidative stress biomarkers, and liver histopathology were assessed. IR resulted in marked histopathology changes in liver tissues coupled with elevations in serum transaminases and liver LDH activities. IR also increased the production of liver lipid peroxides, nitric oxide, and inflammatory cytokines interleukin-1β and interleukin-6, in parallel with a reduction in reduced glutathione and interleukin-10 in the liver. Pretreatment with vinpocetine protected against liver IR-induced injury, in a dose-dependent manner, as evidenced by the attenuation of oxidative stress as well as inflammatory and liver injury biomarkers. The effects of vinpocetine were comparable with that of curcumin, a natural antioxidant, and could be attributed to its antioxidant and anti-inflammatory properties.

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17

Medina, Jesús, and Ricardo Moreno-Otero. "Antioxidant therapy in liver ischemia-reperfusion injury." Liver Transplantation 12, no. 5 (2006): 890–91. http://dx.doi.org/10.1002/lt.20769.

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18

Takhtfooladi, Mohammad Ashrafzadeh, Mehran Shahzamani, Ahmad Asghari, and Aris Fakouri. "Naloxone pretreatment prevents kidney injury after liver ischemia reperfusion injury." International Urology and Nephrology 48, no. 7 (April 7, 2016): 1113–20. http://dx.doi.org/10.1007/s11255-016-1280-5.

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19

Bundzikova, J., Z. Pirnik, L. Lackovicova, B. Mravec, and A. Kiss. "Brain-liver interactions during liver ischemia reperfusion injury: a minireview." Endocrine Regulations 45, no. 3 (2011): 163–72. http://dx.doi.org/10.4149/endo_2011_03_163.

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20

Vasques, E. R., J. E. M. Cunha, A. M. M. Coelho, S. N. Sampietre, R. A. Patzina, H. B. Nader, I. L. S. Tersariol, et al. "Trisulfate disaccharide protects liver injury secondary to liver ischemia/reperfusion." HPB 18 (April 2016): e299. http://dx.doi.org/10.1016/j.hpb.2016.02.766.

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21

Liu, Peitan, Baohuan Xu, John Quilley, and Patrick Y. K. Wong. "Peroxynitrite attenuates hepatic ischemia-reperfusion injury." American Journal of Physiology-Cell Physiology 279, no. 6 (December 1, 2000): C1970—C1977. http://dx.doi.org/10.1152/ajpcell.2000.279.6.c1970.

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In the present study, we examined the effects of peroxynitrite on reperfusion injury using a rat model of hepatic ischemia-reperfusion (HI/R). The left and median lobes of the liver were subjected to 30 min of ischemia, followed by 4 h of reperfusion. Groups A and B rats were sham-operated controls that received vehicle or peroxynitrite; groups C and D rats were subjected to HI/R and received peroxynitrite or vehicle, respectively. A dose of 2 μmol/kg body wt of peroxynitrite, diluted in saline (pH 9.0, 4°C), was administered as a bolus through a portal vein catheter at 0, 60, and 120 min after reperfusion. Results showed that superoxide generation in the ischemic lobes of the liver and plasma alanine aminotransferase (ALT) activity of group C were decreased by 43% and 45%, respectively, compared with group D. Leukocyte accumulations in the ischemic lobes of liver and circulating leukocytes were decreased by 40% and 27%, respectively, in group C vs. D. The ratios of mRNA of P-selectin and intercellular adhesion molecule-1 (ICAM-1) to glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA extracted from the ischemic lobes of the liver of group C were decreased compared with group D. There were no differences between the groups A and B in terms of plasma ALT activity, circulating leukocytes, superoxide generation, and leukocyte infiltration in the ischemic lobes of the liver. Moreover, hemodynamic parameters (i.e., mean arterial blood pressure, cardiac index, stroke index, and systemic vascular resistance) were not significantly different among groups B, C, and D. These results suggest that administration of peroxynitrite via the portal vein only has a local effect. Exogenous peroxynitrite at physiological concentrations attenuates leukocyte-endothelial interaction and reduces leukocyte infiltration. The mechanism of the reduction of leukocyte infiltration into ischemic lobes of the liver appears because of decreased expression of mRNA of P-selectin and ICAM-1. The net effect of administration of peroxynitrite may be to reduce adhesion molecule-mediated, leukocyte-dependent reperfusion injury.

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22

Jiménez-Castro, Mónica B., María Eugenia Cornide-Petronio, Jordi Gracia-Sancho, and Carmen Peralta. "Inflammasome-Mediated Inflammation in Liver Ischemia-Reperfusion Injury." Cells 8, no. 10 (September 23, 2019): 1131. http://dx.doi.org/10.3390/cells8101131.

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Ischemia-reperfusion injury is an important cause of liver damage occurring during surgical procedures including hepatic resection and liver transplantation, and represents the main underlying cause of graft dysfunction and liver failure post-transplantation. To date, ischemia-reperfusion injury is an unsolved problem in clinical practice. In this context, inflammasome activation, recently described during ischemia-reperfusion injury, might be a potential therapeutic target to mitigate the clinical problems associated with liver transplantation and hepatic resections. The present review aims to summarize the current knowledge in inflammasome-mediated inflammation, describing the experimental models used to understand the molecular mechanisms of inflammasome in liver ischemia-reperfusion injury. In addition, a clear distinction between steatotic and non-steatotic livers and between warm and cold ischemia-reperfusion injury will be discussed. Finally, the most updated therapeutic strategies, as well as some of the scientific controversies in the field will be described. Such information may be useful to guide the design of better experimental models, as well as the effective therapeutic strategies in liver surgery and transplantation that can succeed in achieving its clinical application.

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23

Markmann, James F. "Relaxing liver ischemia reperfusion injury down 1 notch." American Journal of Transplantation 18, no. 7 (April 17, 2018): 1587–88. http://dx.doi.org/10.1111/ajt.14741.

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24

Li, Wei-Nan. "Progress in research of liver ischemia-reperfusion injury." World Chinese Journal of Digestology 23, no. 22 (2015): 3554. http://dx.doi.org/10.11569/wcjd.v23.i22.3554.

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25

Lu, Ling, Haoming Zhou, Ming Ni, Xuehao Wang, Ronald Busuttil, Jerzy Kupiec-Weglinski, and Yuan Zhai. "Innate Immune Regulations and Liver Ischemia-Reperfusion Injury." Transplantation 100, no. 12 (December 2016): 2601–10. http://dx.doi.org/10.1097/tp.0000000000001411.

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26

Schemmer, Peter, John J. Lemasters, and Pierre-Alain Clavien. "Ischemia/Reperfusion Injury in Liver Surgery and Transplantation." HPB Surgery 2012 (December 30, 2012): 1. http://dx.doi.org/10.1155/2012/453295.

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27

Marubayashi, S. "Ischemia-reperfusion injury of liver and therapeutic intervention." Hepatology Research 16, no. 3 (February 2000): 233–53. http://dx.doi.org/10.1016/s1386-6346(99)00055-8.

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28

QUIREZEJR, C., E. MONTERO, M. SPERANZINI, L. MARINHO, and A. NIGRO. "36 Apoptosis on ischemia-reperfusion rat liver injury." Liver Transplantation 6, no. 3 (May 2000): C9. http://dx.doi.org/10.1016/s1527-6465(05)80065-6.

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29

Shen, Yuntai, Xiangrong Shen, Yao Cheng, and Yulan Liu. "Myricitrin pretreatment ameliorates mouse liver ischemia reperfusion injury." International Immunopharmacology 89 (December 2020): 107005. http://dx.doi.org/10.1016/j.intimp.2020.107005.

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30

Chazouillères, O., F. Ballet, B. Jolivet, C. Legendre, M. T. Bonnefis, C. Rey, and R. Poupon. "Do bile acids modulate ischemia-reperfusion liver injury?" Journal of Hepatology 11 (January 1990): S17. http://dx.doi.org/10.1016/0168-8278(90)91401-h.

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31

Harki, J., E. J. Kuipers, D. van Noord, H. J. M. Verhagen, and E. T. T. L. Tjwa. "Liver injury is uncommon in chronic gastrointestinal ischemia." European Journal of Internal Medicine 26, no. 5 (June 2015): 369–70. http://dx.doi.org/10.1016/j.ejim.2015.03.003.

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32

Wang, B., M. Bai, Y. Bai, and Q. Li. "Liver Injury Following Renal Ischemia Reperfusion in Rats." Transplantation Proceedings 42, no. 9 (November 2010): 3422–26. http://dx.doi.org/10.1016/j.transproceed.2010.09.008.

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33

Ke, Bibo, Gerald Lipshutz, and Jerzy Kupiec-Weglinski. "Gene Therapy in Liver Ischemia and Reperfusion Injury." Current Pharmaceutical Design 12, no. 23 (August 1, 2006): 2969–75. http://dx.doi.org/10.2174/138161206777947669.

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34

Kincius, M., E. Ryschich, R. Liang, A. Mehrabi, C. Flechtenmacher, M. M. Gebhard, M. W. Büchler, T. W. Kraus, and P. Schemmer. "TAURINE DECREASES INJURY TO LIVER AFTER WARM ISCHEMIA." Transplantation 78 (July 2004): 649. http://dx.doi.org/10.1097/00007890-200407271-01749.

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35

Lim, S. Ping, Fiona J. Andrews, Chris Christophi, and Paul E. O'Brien. "Microvascular changes in liver after ischemia-reperfusion injury." Digestive Diseases and Sciences 39, no. 8 (August 1994): 1683–90. http://dx.doi.org/10.1007/bf02087776.

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36

Lima, Cristiano Xavier, Marcelo Dias Sanches, João Baptista de Rezende Neto, Roberto Carlos de Oliveira e. Silva, Mauro Martins Teixeira, Danielle da Glória de Souza, Guilherme de Castro Santos, and José Renan da Cunha Melo. "Hyperbaric oxygen therapy aggravates liver reperfusion injury in rats." Acta Cirurgica Brasileira 23, no. 4 (August 2008): 315–21. http://dx.doi.org/10.1590/s0102-86502008000400004.

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PURPOSE: To evaluate the effects of hyperbaric oxygen (HO) therapy in the protection against liver ischemia/reperfusion injury. METHODS: Thirty-two male Wistar rats were divided into four groups of eight animals each: group A - laparotomy and liver manipulation, group B - liver ischemia and reperfusion, group C - HO pretreatment for 60 min followed by liver ischemia and reperfusion, and group D - pretreatment with ambient air at 2.5 absolute atmospheres for 60 min followed by liver ischemia and reperfusion. Plasma was assayed for aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH). Intra-arterial blood pressure was monitored continuously. Myeloperoxidase activity in the liver and lung was assessed 30 min after reperfusion. RESULTS: Plasma AST, ALT and LDH increased after reperfusion in all animals. Plasma ALT values and myeloperoxidase activity in the liver parenchyma were higher in HO-pretreated animals than in groups A, B and D. HO had a negative hemodynamic effect during liver reperfusion. CONCLUSION: Liver preconditioning with hyperbaric oxygen therapy aggravated liver ischemia/reperfusion injury in rats as demonstrated by plasma ALT and liver myeloperoxidase activity.

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37

Konishi, Takanori, Rebecca M. Schuster, Holly S. Goetzman, Charles C. Caldwell, and Alex B. Lentsch. "Fibrotic liver has prompt recovery after ischemia-reperfusion injury." American Journal of Physiology-Gastrointestinal and Liver Physiology 318, no. 3 (March 1, 2020): G390—G400. http://dx.doi.org/10.1152/ajpgi.00137.2019.

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Hepatic ischemia-reperfusion (I/R) is a major complication of liver resection, trauma, and liver transplantation; however, liver repair after I/R in diseased liver has not been studied. The present study sought to determine the manner in which the fibrotic liver repairs itself after I/R. Liver fibrosis was established in mice by CCl4 administration for 6 wk, and then liver I/R was performed to investigate liver injury and subsequent liver repair in fibrotic and control livers. After I/R, fibrotic liver had more injury compared with nonfibrotic, control liver; however, fibrotic liver showed rapid resolution of liver necrosis and reconstruction of liver parenchyma. Marked accumulation of hepatic stellate cells and macrophages were observed specifically in the fibrotic septa in early reparative phase. Fibrotic liver had higher numbers of hepatic stellate cells, macrophages, and hepatic progenitor cells during liver recovery after I/R than did control liver, but hepatocyte proliferation was unchanged. Fibrotic liver also had significantly greater number of phagocytic macrophages than control liver. Clodronate liposome injection into fibrotic mice after I/R caused decreased macrophage accumulation and delay of liver recovery. Conversely, CSF1-Fc injection into normal mice after I/R resulted in increased macrophage accumulation and concomitant decrease in necrotic tissue during liver recovery. In conclusion, fibrotic liver clears necrotic areas and restores normal parenchyma faster than normal liver after I/R. This beneficial response appears to be directly related to the increased numbers of nonparenchymal cells, particularly phagocytic macrophages, in the fibrotic liver. NEW & NOTEWORTHY This study is the first to reveal how diseased liver recovers after ischemia-reperfusion (I/R) injury. Although it was not completely unexpected that fibrotic liver had increased hepatic injury after I/R, a novel finding was that fibrotic liver had accelerated recovery and repair compared with normal liver. Enhanced repair after I/R in fibrotic liver was associated with increased expansion of phagocytic macrophages, hepatic stellate cells, and progenitor cells.

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38

Schwabe, Robert F., and David A. Brenner. "Mechanisms of Liver Injury. I. TNF-α-induced liver injury: role of IKK, JNK, and ROS pathways." American Journal of Physiology-Gastrointestinal and Liver Physiology 290, no. 4 (April 2006): G583—G589. http://dx.doi.org/10.1152/ajpgi.00422.2005.

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TNF-α activates several intracellular pathways to regulate inflammation, cell death, and proliferation. In the liver, TNF-α is not only a mediator of hepatotoxicity but also contributes to the restoration of functional liver mass by driving hepatocyte proliferation and liver regeneration. This review summarizes recent advances in TNF-α signaling mechanisms that demonstrate how the IKK, ROS, and JNK pathways interact with each other to regulate hepatocyte apoptosis and proliferation. Activation of these pathways is causatively linked to liver injury induced by concanavalin A, TNF-α, and ischemia-reperfusion and to liver regeneration and hepatocarcinogenesis. In light of recent findings, pharmacological inhibitors of JNK and IKK and antioxidants may be promising new tools for the treatment of hepatitis, ischemia-reperfusion injury, and hepatocellular carcinoma.

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39

Liu, Anding, Wei Dong, Jing Peng, Olaf Dirsch, Uta Dahmen, Haoshu Fang, Cuntai Zhang, and Jian Sun. "Growth differentiation factor 11 worsens hepatocellular injury and liver regeneration after liver ischemia reperfusion injury." FASEB Journal 32, no. 9 (April 17, 2018): 5186–98. http://dx.doi.org/10.1096/fj.201800195r.

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40

Glantzounis, Georgios K., Hemant Sheth, Cecil Thompson, Tariq S. Hafez, Sanjeev Kanoria, Viniyendra Pamecha, Susan Davies, Dimitri P. Mikhailidis, Alexander M. Seifalian, and Brian R. Davidson. "Acute Limb Ischemia Caused by Femoral Arterial Line Induces Remote Liver Injury in a Rabbit Model of Liver Ischemia/Reperfusion Injury." Angiology 60, no. 5 (July 21, 2009): 554–61. http://dx.doi.org/10.1177/0003319709338176.

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Femoral arterial lines are used for continuous monitoring of arterial blood pressure in experimental studies. However, placement of a catheter in the femoral artery could produce acute limb ischemia with associated systemic effects. The aim of this study was to investigate the effect of femoral arterial line insertion on liver function, in a rabbit liver lobar ischemia-reperfusion (I/R) model. Four groups of animals (n = 6 each) were studied: groups 1 and 2 (sham) underwent laparotomy but no liver ischemia. In groups 3 and 4 (I/R), liver lobar ischemia was induced for 60 minutes followed by 7 hours of reperfusion. In groups 1 and 3, the arterial line was placed in the femoral artery whereas in groups 2 and 4 in the ear artery. Liver function was assessed by serum alanine aminotransferase (ALT) activity, bile flow, plasma lactate levels, and histology. Results are expressed as mean ± SEM. Alanine aminotransferase activity and lactate levels were significantly higher in the I/R femoral line group compared with the I/R ear line group at 7 hours postreperfusion. Bile production was significantly lower (75 ± 9.6 vs 112 ± 10 μL/min per 100 g liver weight). Histopathology showed more extensive hepatocellular necrosis and neutrophil accumulation in the I/R femoral line group compared with I/R ear line group. The sham femoral group showed liver injury, which was more marked than the ear line group (all P < .05). In conclusion, femoral artery cannulation induces remote liver injury. The use of femoral arterial lines should be avoided in experimental studies concerning liver function.

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41

Liu, Hongqiang, Ying Yuan, and Dan Rao. "Sevoflurane alleviates liver ischemia reperfusion injury through inactivation of the TRAF6/NF-κB signaling pathway." Tropical Journal of Pharmaceutical Research 20, no. 10 (November 20, 2021): 2043–48. http://dx.doi.org/10.4314/tjpr.v20i10.5.

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Purpose: To evaluate the role and mechanism of action of sevoflurane in liver ischemia reperfusion injury.Methods: Rats were pretreated with sevoflurane and then underwent liver ischemia followed by reperfusion to establish an animal model of liver ischemia reperfusion injury. Pathological changes in liver tissues were investigated by hematoxylin and eosin (H & E) staining, and serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were determined using a chemistryanalyzer. ELISA was used to determine the levels of myeloperoxidase (MPO), tumor necrosis factor-α (TNF-α), interleukin-1 beta (IL-1β), IL-6, superoxide (SOD), malonaldehyde (MDA), catalase (CAT), and glutathione (GSH).Results: Pathological changes in liver tissue, including sinusoidal congestion, vacuole formation, and infiltration of inflammatory cells and lymphocytes, were identified in rats post-ischemia reperfusion injury. In addition, serum ALT and AST levels increased following ischemia reperfusion injury. However, administration of sevoflurane ameliorated the pathological liver damage and decreased the serum ALTand AST levels induced by ischemia reperfusion. Pro- inflammatory cytokines, such as MPO, TNF-α, IL- 1β, and IL-6 were upregulated in rats following ischemia reperfusion injury, and this upregulation was reversed by sevoflurane administration. Sevoflurane administration also attenuated the ischemia reperfusion-induced increase in MDA and decrease in SOD, CAT, and GSH. Ischemia reperfusionrepressed IκBα protein expression and promoted protein expression of TNF receptor associated factor 6 (TRAF6), phospho (p)-IκBα, and p-p65 in liver tissue. However, sevoflurane reversed the effect of ischemia reperfusion on IκBα, TRAF6, p-IκBα, and p-65 expression.Conclusion: Sevoflurane administration reduced pathological liver injury post-ischemia reperfusion bysuppressing the inflammatory response and oxidative stress through inactivation of the TRAF6/NF-κB pathway.

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42

Weigand, Kilian, Sylvia Brost, Niels Steinebrunner, Markus Büchler, Peter Schemmer, and Martina Müller. "Ischemia/Reperfusion Injury in Liver Surgery and Transplantation: Pathophysiology." HPB Surgery 2012 (May 30, 2012): 1–8. http://dx.doi.org/10.1155/2012/176723.

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Liver ischemia/reperfusion (IR) injury is caused by a heavily toothed network of interactions of cells of the immune system, cytokine production, and reduced microcirculatory blood flow in the liver. These complex networks are further elaborated by multiple intracellular pathways activated by cytokines, chemokines, and danger-associated molecular patterns. Furthermore, intracellular ionic disturbances and especially mitochondrial disorders play an important role leading to apoptosis and necrosis of hepatocytes in IR injury. Overall, enhanced production of reactive oxygen species, found very early in IR injury, plays an important role in liver tissue damage at several points within these complex networks. Many contributors to IR injury are only incompletely understood so far. This paper tempts to give an overview of the different mechanisms involved in the formation of IR injury. Only by further elucidation of these complex mechanisms IR injury can be understood and possible therapeutic strategies can be improved or be developed.

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43

Ma, Wen, Songling Tang, Dina Xie, Guoqiang Gu, and Lu Gan. "The Protective Effect of Traditional Chinese Medicine on Liver Ischemia-Reperfusion Injury." Evidence-Based Complementary and Alternative Medicine 2021 (April 8, 2021): 1–5. http://dx.doi.org/10.1155/2021/5564401.

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Abstract:

Liver ischemia-reperfusion (I/R) injury occurs during transplantation and major hepatic surgery, which may lead to postoperative liver dysfunction. More and more traditional Chinese medicines (TCMs) have been used to treat liver ischemia-reperfusion injury. The purpose of this review is to evaluate the different protective effects of TCMs in the treatment of liver ischemia-reperfusion injury and to summarize its possible mechanisms. The results indicate that TCMs attenuate liver I/R injury via multiple mechanisms, including antioxidation stress, anti-inflammatory response, antiapoptosis, and inhibiting endoplasmic reticulum stress. However, the in-depth mechanism of the protective effects of these traditional Chinese medicines still remains unknown.

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Qi, Shunli, Qi Yan, Zhen Wang, Deng Liu, Mengting Zhan, Jian Du, and Lijian Chen. "Oleoylethanolamide Alleviates Hepatic Ischemia-Reperfusion Injury via Inhibiting Endoplasmic Reticulum Stress-Associated Apoptosis." PPAR Research 2022 (March 21, 2022): 1–14. http://dx.doi.org/10.1155/2022/2212996.

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Liver ischemia/reperfusion (I/R) injury is a primary complication in major liver surgery. Our previous study about proteome profiling has revealed that the PPAR signaling cascade was significantly upregulated during liver ischemia/reperfusion. To elucidate the potential mechanisms of PPARα involved in I/R injury, we used oleoylethanolamide (OEA), the peroxisome proliferator-activated receptor alpha (PPARα) agonist, in this study. We demonstrated a protective role of OEA on liver I/R injury by using a mouse model of partial warm ischemia-reperfusion and hypoxia-reoxygenation model of hepatocytes. These effects were caused by ameliorating liver damage, decreasing the level of serum ALT and AST, and reducing the apoptosis of hepatocytes. Furthermore, a mechanistic study revealed that OEA regulated endoplasmic reticulum (ER) stress by activating PPARα, thereby reducing ER stress-associated apoptosis to attenuate liver I/R injury. Briefly, these data first proposed that OEA-mediated PPARα activation could be an effective therapy against hepatic ischemia/reperfusion injury.

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Xing, Hui-chun, Lan-juan Li, Kai-jin Xu, Tian Shen, Yun-bo Chen, Ji-fang Sheng, Yun-song Yu, and Ya-gang Chen. "Intestinal microflora in rats with ischemia/reperfusion liver injury." Journal of Zhejiang University SCIENCE 6B, no. 1 (January 2005): 14–21. http://dx.doi.org/10.1631/jzus.2005.b0014.

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Takasu, Chie, Nosratola D. Vaziri, Shiri Li, Lourdes Robles, Kelly Vo, Mizuki Takasu, Christine Pham, et al. "Treatment with dimethyl fumarate ameliorates liver ischemia/reperfusion injury." World Journal of Gastroenterology 23, no. 25 (2017): 4508. http://dx.doi.org/10.3748/wjg.v23.i25.4508.

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Arkadopoulos, Nikolaos, Constantinos Nastos, Konstantinos Kalimeris, Emmanuil Economou, Kassiani Theodoraki, Evangelia Kouskouni, Agathi Pafiti, Georgia Kostopanagiotou, and Vassilios Smyrniotis. "Iron Chelation for Amelioration of Liver Ischemia-Reperfusion Injury." Hemoglobin 34, no. 3 (June 2010): 265–77. http://dx.doi.org/10.3109/03630269.2010.484766.

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Zimmerman, Michael, Alicia Martin, Jennifer Yee, Jennifer Schiller, and Johnny Hong. "Natural Killer T Cells in Liver Ischemia–Reperfusion Injury." Journal of Clinical Medicine 6, no. 4 (April 1, 2017): 41. http://dx.doi.org/10.3390/jcm6040041.

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Wang, Cheng-You. "Mild hypothermia protects liver against ischemia and reperfusion injury." World Journal of Gastroenterology 11, no. 19 (2005): 3005. http://dx.doi.org/10.3748/wjg.v11.i19.3005.

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Mota-Filipe, Helder. "ROLE OF PARP IN THE LIVER ISCHEMIA-REPERFUSION INJURY." Shock 21, Supplement (March 2004): 91. http://dx.doi.org/10.1097/00024382-200403001-00364.

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