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Journal articles on the topic 'Modello ischemia in vitro'

Author: Grafiati

Published: 9 March 2023

Last updated: 10 March 2023

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1

Pelliccioli, G. P., P. F. Ottaviano, C. Gambelunghe, G. Mariucci, G. Bruschelli, G. Bartoli, and M. V. Ambrosini. "Ischemia cerebrale sperimentale nei gerbillo." Rivista di Neuroradiologia 6, no. 3 (August 1993): 325–30. http://dx.doi.org/10.1177/197140099300600313.

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Il gerbillo (Meriones unguiculatus), avendo il circolo di Willis incompleto per la mancanza delle arterie comunicanti, è considerato il modello animale di elezione per lo studio dell'ischemia cerebrale. L'assenza di connessioni tra circolo carotideo e vertebro-basilare garantisce infatti l'induzione di un'ischemia cerebrale mediante occlusione delle arterie carotidi comuni (ACC). È stata osservata tuttavia una certa variabilità nel sistema vascolare cerebrale del gerbillo, che spiegherebbe la differente risposta individuale alla legatura delle ACC. In letteratura sono stati descritti i deficit funzionali e le modificazioni comportamentali secondari ad un'ischemia cerebrale, correlabili post mortem a definiti quadri istopatologici. Raramente sono stati applicati metodi certi di valutazione in vivo degli esiti di un'ischemia cerebrale sperimentale e/o dell'efficacia di eventuali interventi terapeutici. Un contributo alle indagini in vivo sull'ischemia cerebrale sperimentale potrebbe derivare dallo studio con risonanza magnetica. La nostra indagine ha avuto lo scopo di valutare alla RM, l'evoluzione e la gravità del danno prodotto nel gerbillo: a) dall'occlusione di entrambe le ACC per 5 mine (b) dalla legatura permanente di una ACC. Lo studio parenchimale ed angiografico è stato condotto utilizzando apparecchiature da 1,5 Tesla. Gli animali sono stati esaminati a tempi diversi dall'ischemia. L'iperintensità del segnale rilevata in alcuni casi con le sequenze spin echo a TR lungo a carico dell'ippocampo non era semprecorrelabile al tipo di ischemia indotta. In un 20% dei casi si è apprezzato un aumento di volume del sistema ventricolare, confermato dall'esame anatomo-patologico. Lo studio istologico ha dimostrato che l'aumento di intensità del segnale non era obbligatoriamente associato a severi danni del parenchima. I risultati di questo studio, seppure preliminare, sosterrebbero la validità della tecnica RM nello studio delle ischemie cerebrali sperimentali, poiché essa consente di individuare un edema nel tessuto ischemico anche in assenza di grave sofferenza e/o necrosi cellulare. Le differenti risposte del gerbillo all'ischemia cerebrale potrebbero essere dovute ad una variabilita sia anatomica che biologica.

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2

Visocchi, M., M. Meglio, D. Cabezas Cuevas, B. Cioni, P. Carducci, G. Mastroianni, T. Tartaglione, G. Di Lella, and C. Colosimo. "Sensibilità e specificità della RM in un nuovo modello di ictus ischemico acuto sperimentale «collaterale»." Rivista di Neuroradiologia 9, no. 1 (February 1996): 21–23. http://dx.doi.org/10.1177/197140099600900102.

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Al fine di valutare la precocità e la sensibilità diagnostica della RM, unitamente alla eventuale ripetibilità degli eventi, abbiamo voluto sperimentare un nuovo modello di ischemia, che abbiamo definito «collaterale», poichè secondaria ad occlusione di due o più vasi pre - Willisiani. Per l'analogia con il circolo cerebrale umano sono stati studiati 12 conigli albini New Zealand (4–5 Kg) che venivano sottoposti ad anestesia generale. Per tutta la durata dell'esperimento si procedeva al monito-raggio della pressione arteriosa sistemica media, della frequenza cardiaca del pH e dell'emogas. L'ischemia veniva indotta con tecnica microchirurgica in 8 animali mediante chiusura di entrambe le carotidi comuni al collo (durata da un minimo di 2 h ad un massimo di 24 h) ed in altri 4 mediante chiusura dei vasi epiaor-tici a livello dell'arco aortico (durata da un minimo di 2 h ad un massimo di 4h). L'animale veniva sacrifi-cato senza previa riperfusione. Veniva quindi eseguito in tutti gli animali uno studio RM. In un caso (#12) il danno non è stato valutabile per la scarsa qualità iconografica. In otto casi sono state chiaramente iden-tificate incostanti e sfumate immagini lesionali lineari e/o puntiformi, prevalentemente monolaterali e a sede variabile. In analogia con quanto dimostrato in alcuni modelli di ischemia «terminale» studiati con RM, nel nostro gruppo di animali il danno ischemico «collaterale» è già evidente entro le prime due ore sia con chiusure di entrambe le carotidi che dell'arco aortico. La povertà dei reperti ottenuti, la aspecificità degli stessi, forse legata ad una vulnerabilità selettiva al-Pipossia di alcune strutture cerebrali mesiali e la scarsa ripetibilità degli stessi, scoraggia l'impiego del modello in oggetto per uno studio sistematico sperimentale dell'ischemia e quindi dell'efficacia di trials tera-peutici, sebbene la stessa negatività dello studio RM non possa escludere completamente un danno ischemico neuronale.

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3

Chen, Timothy, and Gordana Vunjak-Novakovic. "In Vitro Models of Ischemia-Reperfusion Injury." Regenerative Engineering and Translational Medicine 4, no. 3 (May 11, 2018): 142–53. http://dx.doi.org/10.1007/s40883-018-0056-0.

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4

Dugan, Laura L., and Jeong-Sook Kim-Han. "Astrocyte Mitochondria in In Vitro Models of Ischemia." Journal of Bioenergetics and Biomembranes 36, no. 4 (August 2004): 317–21. http://dx.doi.org/10.1023/b:jobb.0000041761.61554.44.

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5

Lee, Won Hee, Sungkwon Kang, Pavlos P. Vlachos, and Yong Woo Lee. "A novel in vitro ischemia/reperfusion injury model." Archives of Pharmacal Research 32, no. 3 (March 2009): 421–29. http://dx.doi.org/10.1007/s12272-009-1316-9.

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6

Tanaka, E., S. Yasumoto, G. Hattori, S. Niiyama, S. Matsuyama, and H. Higashi. "Mechanisms Underlying the Depression of Evoked Fast EPSCs Following In Vitro Ischemia in Rat Hippocampal CA1 Neurons." Journal of Neurophysiology 86, no. 3 (September 1, 2001): 1095–103. http://dx.doi.org/10.1152/jn.2001.86.3.1095.

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The mechanisms underlying the depression of evoked fast excitatory postsynaptic currents (EPSCs) following superfusion with medium deprived of oxygen and glucose (in vitro ischemia) for a 4-min period in hippocampal CA1 neurons were investigated in rat brain slices. The amplitude of evoked fast EPSCs decreased by 85 ± 7% of the control 4 min after the onset of in vitro ischemia. In contrast, the exogenous glutamate-induced inward currents were augmented, while the spontaneous miniature EPSCs obtained in the presence of tetrodotoxin (TTX, 1 μM) did not change in amplitude during in vitro ischemia. In a normoxic medium, a pair of fast EPSCs was elicited by paired-pulse stimulation (40-ms interval), and the amplitude of the second fast EPSC increased to 156 ± 24% of the first EPSC amplitude. The ratio of paired-pulse facilitation (PPF ratio) increased during in vitro ischemia. Pretreatment of the slices with adenosine 1 (A1) receptor antagonist, 8-cyclopenthyltheophiline (8-CPT) antagonized the depression of the fast EPSCs, in a concentration-dependent manner: in the presence of 8-CPT (1–10 μM), the amplitude of the fast EPSCs decreased by only 20% of the control during in vitro ischemia. In addition, 8-CPT antagonized the enhancement of the PPF ratio during in vitro ischemia. A pair of presynaptic volleys and excitatory postsynaptic field potentials (fEPSPs) were extracellularly recorded in a proximal part of the stratum radiatum in the CA1 region. The PPF ratio for the fEPSPs also increased during in vitro ischemia. On the other hand, the amplitudes of the first and second presynaptic volley, which were abolished by TTX (0.5 μM), did not change during in vitro ischemia. The maximal slope of the Ca2+-dependent action potential of the CA3 neurons, which were evoked in the presence of 8-CPT (1 μM), nifedipine (20 μM), TTX (0.5 μM), and tetraethyl ammonium chloride (20 mM), decreased by 12 ± 6% of the control 4 min after the onset of in vitro ischemia. These results suggest that in vitro ischemia depresses the evoked fast EPSCs mainly via the presynaptic A1 receptors, and the remaining 8-CPT–resistant depression of the fast EPSCs is probably due to a direct inhibition of the Ca2+ influx to the axon terminals.

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7

Ke, Yong-Sheng, He-Gui Wang, De-Guo Wang, and Gen-Bao Zhang. "Endoxin-mediated myocardial ischemia reperfusion injury in rats in vitro." Canadian Journal of Physiology and Pharmacology 82, no. 6 (May 1, 2004): 402–8. http://dx.doi.org/10.1139/y04-041.

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Myocardial ischemia reperfusion results in an increase in intracellular sodium concentration, which secondarily increases intracellular calcium via Na+-Ca2+ exchange, resulting in cellular injury. Endoxin is an endogenous medium of digitalis receptor and can remarkably inhibit Na+/K+-ATPase activity. Although the level of plasma endoxin is significantly higher during myocardial ischemia, its practical significance is unclear. This research is to investigate whether endoxin is one of important factors involved in myocardial ischemia reperfusion injury. Ischemia reperfusion injury was induced by 30 min of global ischemia and 30 min of reperfusion in isolated rat hearts. Heart rate (HR), left ventricular developed pressure (LVDP), and its first derivative (±dp/dtmax) were recorded. The endoxin contents, intramitochondrial Ca2+ contents, and the Na+/K+-ATPase activity in myocardial tissues were measured. Myocardial damages were evaluated by electron microscopy. The endoxin and intramitochondrial Ca2+ contents in myocardial tissues were remarkably higher, myocardial membrane ATPase activity was remarkably lower, the cardiac function was significantly deteriorated, and myocardial morphological damages were severe in myocardial ischemia reperfusion group vs. control. Anti-digoxin antiserum (10, 30 mg/kg) caused a significant improvement in cardiac function (LVDP and ±dp/dtmax), Na+/K+-ATPase activity, and myocardial morphology, and caused a reduction of endoxin and intramitochondrial Ca2+ contents in myocardial tissues. In the present study, the endoxin antagonist, anti-digoxin antiserum, protected the myocardium against the damages induced by ischemia reperfusion in isolated rat hearts. The results suggest that endoxin might be one of main factors mediating myocardial ischemia reperfusion injury.Key words: endoxin, anti-digoxin antiserum, myocardial reperfusion injury, morphological evaluation, Na+/K+-exchanging ATPase.

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8

Joshi, Dhiraj, Hemanshu Patel, Daryll M. Baker, Xu Shiwen, David J. Abraham, and Janice C. Tsui. "Development of an in vitro model of myotube ischemia." Laboratory Investigation 91, no. 8 (May 23, 2011): 1241–52. http://dx.doi.org/10.1038/labinvest.2011.79.

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9

Richard, Marc J. P., Tarek M. Saleh, Bouchaib El Bahh, and Jeffrey A. Zidichouski. "A novel method for inducing focal ischemia in vitro." Journal of Neuroscience Methods 190, no. 1 (June 2010): 20–27. http://dx.doi.org/10.1016/j.jneumeth.2010.04.017.

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10

Maher, Pamela, and Anne Hanneken. "Flavonoids protect retinal ganglion cells from ischemia in vitro." Experimental Eye Research 86, no. 2 (February 2008): 366–74. http://dx.doi.org/10.1016/j.exer.2007.11.009.

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11

van Griensven, Martijn, Michael Stalp, and Andreas Seekamp. "ISCHEMIA-REPERFUSION DIRECTLY INCREASES PULMONARY ENDOTHELIAL PERMEABILITY IN VITRO." Shock 11, no. 4 (April 1999): 259–63. http://dx.doi.org/10.1097/00024382-199904000-00006.

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12

Chandrasekaran, Krishnaswamy, James F. Greenleaf, Brent S. Robinson, William D. Edwards, James B. Seward, and A. Jamil Tajik. "Echocardiographic visualization of acute myocardial ischemia—In vitro study." Ultrasound in Medicine & Biology 12, no. 10 (October 1986): 785–93. http://dx.doi.org/10.1016/0301-5629(86)90076-1.

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13

Schurr, Avital, Ralphiel S. Payne, Kenneth H. Reid, Vasudeva Iyer, Michael T. Tseng, Manlei M. Li, Shyue-An Chan, Caroline Young, James J. Miller, and Benjamin M. Rigor. "Cardiac arrest-induced global cerebral ischemia studied in vitro." Life Sciences 57, no. 26 (November 1995): 2425–30. http://dx.doi.org/10.1016/0024-3205(95)02238-7.

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14

Prehn, Jochen H. M., Chourouk Karkoutly, Jörg Nuglisch, Barbara Peruche, and Josef Krieglstein. "Dihydrolipoate Reduces Neuronal Injury after Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 12, no. 1 (January 1992): 78–87. http://dx.doi.org/10.1038/jcbfm.1992.10.

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It has been shown in vitro that dihydrolipoate (dl-6,8-dithioloctanoic acid) has antioxidant activity against microsomal lipid peroxidation. We tested dihydrolipoate for its neuroprotective activity using models of hypoxic and excitotoxic neuronal damage in vitro and rodent models of cerebral ischemia in vivo. In vitro, neuronal damage was induced in primary neuronal cultures derived form 7-day-old chick embryo telencephalon by adding either 1 m M cyanide or 1 m M glutamate to the cultures. Cyanide-exposed and dihydrolipoate-treated (10−9–10−7 M) cultures showed an increased protein and ATP content compared with controls. The glutamate-exposed cultures treated with dihydrolipoate (10−7–10−5 M) showed a decreased number of damaged neurons. In vivo, dihydrolipoate treatment (50 and 100 mg/kg) reduced brain infarction after permanent middle cerebral artery occlusion in mice and rats. Dihydrolipoate treatment (50 and 100 mg/kg) could not ameliorate neuronal damage in the rat hippocampus or cortex caused by 10 min of forebrain ischemia. A comparable neuroprotection was obtained by using dimethylthiourea, both in vitro (10−7 and 10−6 M) and at a dose of 750 mg/kg in the focal ischemia models. Lipoate, the oxidized form of dihydrolipoate, failed to reduce neuronal injury in any model tested. We conclude that dihydrolipoate, similarly to dimethylthiourea, is able to protect neurons against ischemic damage by diminishing the accumulation of reactive oxygen species within the cerebral tissue.

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15

Shin, Tae Hwan, Da Yeon Lee, Shaherin Basith, Balachandran Manavalan, Man Jeong Paik, Igor Rybinnik, M. Maral Mouradian, Jung Hwan Ahn, and Gwang Lee. "Metabolome Changes in Cerebral Ischemia." Cells 9, no. 7 (July 7, 2020): 1630. http://dx.doi.org/10.3390/cells9071630.

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Cerebral ischemia is caused by perturbations in blood flow to the brain that trigger sequential and complex metabolic and cellular pathologies. This leads to brain tissue damage, including neuronal cell death and cerebral infarction, manifesting clinically as ischemic stroke, which is the cause of considerable morbidity and mortality worldwide. To analyze the underlying biological mechanisms and identify potential biomarkers of ischemic stroke, various in vitro and in vivo experimental models have been established investigating different molecular aspects, such as genes, microRNAs, and proteins. Yet, the metabolic and cellular pathologies of ischemic brain injury remain not fully elucidated, and the relationships among various pathological mechanisms are difficult to establish due to the heterogeneity and complexity of the disease. Metabolome-based techniques can provide clues about the cellular pathologic status of a condition as metabolic disturbances can represent an endpoint in biological phenomena. A number of investigations have analyzed metabolic changes in samples from cerebral ischemia patients and from various in vivo and in vitro models. We previously analyzed levels of amino acids and organic acids, as well as polyamine distribution in an in vivo rat model, and identified relationships between metabolic changes and cellular functions through bioinformatics tools. This review focuses on the metabolic and cellular changes in cerebral ischemia that offer a deeper understanding of the pathology underlying ischemic strokes and contribute to the development of new diagnostic and therapeutic approaches.

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16

He, Yangdong, Ya Hua, Wenquan Liu, Haitao Hu, Richard F. Keep, and Guohua Xi. "Effects of Cerebral Ischemia on Neuronal Hemoglobin." Journal of Cerebral Blood Flow & Metabolism 29, no. 3 (December 10, 2008): 596–605. http://dx.doi.org/10.1038/jcbfm.2008.145.

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This study examined whether neuronal hemoglobin (Hb) is present in rats. It then examined whether cerebral ischemia or ischemic preconditioning (IPC) affects neuronal Hb levels in vivo and in vitro. In vivo, male Sprague-Dawley rats were subjected to either 15 mins of transient middle cerebral artery occlusion (MCAO) with 24 h of reperfusion, an IPC stimulus, or 24 h of permanent MCAO (pMCAO), or IPC followed 3 days later by 24 h of pMCAO. In vitro, primary cultured neurons were exposed to 2 h of oxygen—glucose deprivation (OGD) with 22 h of reoxygenation. Results showed that Hb is widely expressed in rat cerebral neurons but not astrocytes. Hemoglobin expression was significantly upregulated in the ipsilateral caudate and the cortical core of the middle cerebral artery territory after IPC. Hemoglobin levels also increased more in the penumbral cortex and the contralateral hemisphere 24 h after pMCAO, but expressions in the ipsilateral caudate and the cortical core area were decreased. Ischemic preconditioning modified pMCAO-induced brain Hb changes. Neuronal Hb levels in vitro were increased by 2 h of OGD and 22 h of reoxygenation. These results indicate that Hb is synthesized in neurons and can be upregulated by ischemia.

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17

Jamarkattel-Pandit, Nirmala, and Hocheol Kim. "Neuroprotective Effect of Metaplexis japonica against in vitro Ischemia Model." Journal of Health and Allied Sciences 3, no. 1 (November 24, 2019): 51–55. http://dx.doi.org/10.37107/jhas.55.

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Metaplexis japonica (Apocynaceae) is a perennial herb, extensively used in traditional medicinal system for various diseases. The purpose of the study was to evaluate the protective effect of M. japonica against in vitro ischemia. In the present study, 70% ethanol extract of M. japonica was fractionated with different polarity solvents. For in vitro ischemia, oxygen-glucose deprivation followed by reoxygenation (OGD-R) in cells was used to investigate the effects of M. japonica and its fractions. For oxidative stress model, Hydrogen peroxide (H2 O2 ) induced cell death was studied in HT22 cell line. M. japonica and its fractions significantly reduced the HT22 cell damage, which was induced by 4 hrs of OGD followed by 24 hrs of reoxygenation and 24 hrs of H2 O2, respectively. The effectiveness of ethyl acetate fraction was higher than other fractions/crude extract. Our results suggest that M. japonica could be a neuroprotective agent for the treatment of stroke. Key words: Metaplexis japonica, Stroke, Oxygen-glucose deprivation, Neuroprotection

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18

Walsh, L. G., and J. M. Tormey. "Subcellular electrolyte shifts during in vitro myocardial ischemia and reperfusion." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 4 (October 1, 1988): H917—H928. http://dx.doi.org/10.1152/ajpheart.1988.255.4.h917.

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Isolated perfused rabbit right ventricular wall was studied with electron probe microanalysis (EPMA) under three conditions: 1) control (37 degrees C, 1.2 Hz), 2) 60 min global ischemia, and 3) ischemia plus 5 min of reperfusion. After 60 min of ischemia, only one cell population was evident; the variance of intracellular electrolyte concentrations was the same as in controls. When compared with controls, there was no change in Ca concentration within any region of the cell, but mitochondria were swollen with K-rich fluid. Two cell populations were evident after 5 min of reperfusion. The severely injured cells were markedly swollen, exhibited hypercontraction bands, and had electrolyte profiles similar to extracellular fluid. The moderately injured cells were normal in appearance, still retained electrolyte gradients, but had elevated Na and Cl concentrations in all compartments. Cell Ca did not increase in the moderately injured cells, but the region of the cell containing the sarcoplasmic reticulum (SR) lost 90% of its Ca. Accompanying this loss were large increases in myofibrillar and mitochondrial Ca concentration. It appears that release of SR Ca, loss of SR Ca-accumulating capacity, and increased intracellular Na are the principal electrolyte shifts in functional cells during early reperfusion.

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19

Han, Moon-Ku, Manho Kim, So Yon Bae, Lami Kang, So Young Han, Yong-Seok Lee, Jeong Ho Rha, Seung U. Kim, and Jae-Kyu Roh. "VEGF protects human cerebral hybrid neurons from in vitro ischemia." NeuroReport 15, no. 5 (April 2004): 847–50. http://dx.doi.org/10.1097/00001756-200404090-00022.

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20

Russ, Alissa L., Karen M. Haberstroh, and Ann E. Rundell. "Experimental strategies to improve in vitro models of renal ischemia." Experimental and Molecular Pathology 83, no. 2 (October 2007): 143–59. http://dx.doi.org/10.1016/j.yexmp.2007.03.002.

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21

Inauen, W., D. N. Granger, C. J. Meininger, M. E. Schelling, H. J. Granger, and P. R. Kvietys. "An in vitro model of ischemia/reperfusion-induced microvascular injury." American Journal of Physiology-Gastrointestinal and Liver Physiology 259, no. 1 (July 1, 1990): G134—G139. http://dx.doi.org/10.1152/ajpgi.1990.259.1.g134.

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The major objective of this study was to develop an in vitro model of ischemia/reperfusion (I/R)-induced microvascular injury. Cultured venular endothelial cells were grown to confluency, labeled with 51Cr, and exposed to different durations of anoxia (0.5, 1, 2, 3, and 4 h). 51Cr release and cell detachment (indexes of cell injury) were determined at different times after reoxygenation (1, 2, 4, 6, 8, and 18 h). Because in vivo studies have implicated neutrophils in I/R injury, in some experiments human neutrophils were added to the endothelial cells upon reoxygenation. Periods of anoxia greater than or equal to 2 h resulted in 70-80% 51Cr release and 80-95% cell detachment upon reoxygenation. Under these conditions (near maximal injury), the addition of neutrophils produced negligible effects. Periods of anoxia less than or equal to 1 h resulted in 30-40% 51Cr release and 50-60% cell detachment. Under these conditions (moderate cell injury), addition of neutrophils enhanced endothelial cell injury. Using a 30-min period of anoxia, we also assessed the effects of superoxide dismutase (SOD; 300 U/ml) and allopurinol (20 microM) on anoxia/reoxygenation (A/R)-induced injury in the presence or absence of neutrophils. In the absence of neutrophils, SOD or allopurinol did not protect against A/R-induced injury. However, in the presence of neutrophils, both SOD and allopurinol attenuated the increases in 51Cr release. The results derived using this in vitro model of I/R injury are largely consistent with published in vivo studies. Thus this in vitro model may provide further insights regarding the mechanisms involved in I/R injury.

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22

Dmitriev, Ruslan I., and Dmitri B. Papkovsky. "In vitro ischemia decreases histone H4K16 acetylation in neural cells." FEBS Letters 589, no. 1 (December 3, 2014): 138–44. http://dx.doi.org/10.1016/j.febslet.2014.11.038.

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23

Ye, Zhouheng, Bradley P. Ander, Frank R. Sharp, and Xinhua Zhan. "Cleaved β-Actin May Contribute to DNA Fragmentation Following Very Brief Focal Cerebral Ischemia." Journal of Neuropathology & Experimental Neurology 77, no. 3 (February 2, 2018): 260–65. http://dx.doi.org/10.1093/jnen/nly003.

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Abstract Our previous study demonstrated caspase independent DNA fragmentation after very brief cerebral ischemia, the mechanism of which was unclear. In this study, we explore whether actin is cleaved following focal cerebral ischemia, and whether these structural changes of actin might modulate DNA fragmentation observed following focal ischemia. Results showed that a cleaved β-actin fragment was identified in brains of rats 24 hours following 10-minute and 2-hour focal ischemia. Though granzyme B and caspase-3 cleaved β-actin in vitro, the fragment size of β-actin cleaved by granzyme B was the same as those found after 10-minute and 2-hour focal ischemia. This was consistent with increases of granzyme B activity after 10-minute and 2-hour ischemia compared with controls. Cerebral extracts from 10-minute and 2-hour ischemic brains degraded DNA in vitro. Adding intact β-actin to these samples completely abolished DNA degradation from the 10-minute ischemia group but not from the 2-hour ischemia group. We concluded that β-actin is likely cleaved by granzyme B by 24 hours following 10-minute and 2-hour focal cerebral ischemia. Intact β-actin inhibits DNase, and cleavage of β-actin activates DNase, which leads to DNA fragmentation observed in the brain following very brief focal ischemia.

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24

Jurcau, Anamaria, and Aurel Simion. "Neuroinflammation in Cerebral Ischemia and Ischemia/Reperfusion Injuries: From Pathophysiology to Therapeutic Strategies." International Journal of Molecular Sciences 23, no. 1 (December 21, 2021): 14. http://dx.doi.org/10.3390/ijms23010014.

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Its increasing incidence has led stroke to be the second leading cause of death worldwide. Despite significant advances in recanalization strategies, patients are still at risk for ischemia/reperfusion injuries in this pathophysiology, in which neuroinflammation is significantly involved. Research has shown that in the acute phase, neuroinflammatory cascades lead to apoptosis, disruption of the blood–brain barrier, cerebral edema, and hemorrhagic transformation, while in later stages, these pathways support tissue repair and functional recovery. The present review discusses the various cell types and the mechanisms through which neuroinflammation contributes to parenchymal injury and tissue repair, as well as therapeutic attempts made in vitro, in animal experiments, and in clinical trials which target neuroinflammation, highlighting future therapeutic perspectives.

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25

Hillered, Lars, Maj-Lis Smith, and Bo K. Siesjö. "Lactic Acidosis and Recovery of Mitochondrial Function following Forebrain Ischemia in the Rat." Journal of Cerebral Blood Flow & Metabolism 5, no. 2 (June 1985): 259–66. http://dx.doi.org/10.1038/jcbfm.1985.33.

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The effect of different degrees of lactic acidosis on the recovery of brain mitochondrial function, measured as respiratory activity in isolated mitochondria or cortical concentrations of labile phosphates and carbohydrate substrates, was studied during 30 min of recirculation following 15 min of near-complete forebrain ischemia in rats. During ischemia, there was a marked decrease in mitochondrial State 3 respiration in vitro and a depletion of energy stores (i.e., phosphocreatine, ATP, glucose, and glycogen) in vivo that was similar in the high- and low-lactate ischemia groups. However, lactate concentrations differed markedly (20 and 10 μmol g−1, respectively). During recirculation, there was a near-complete recovery of both respiratory activity in vitro and adenylate energy charge (EC) in vivo regardless of the differences in lactic acidosis during ischemia. Respiratory activity and EC were well correlated. The changes in Ca2+ homeostasis during ischemia, an increase in tissue and a decrease in mitochondrial Ca2+ content, were reversed rapidly after ischemia in both high- and low-lactate ischemia animals and did not hinder an early recovery of mitochondrial function. It is concluded that lactic acidosis, with lactate levels reaching 20 μmol g−1 during 15-min ischemia, does not adversely affect early postischemic recovery of mitochondrial function.

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26

Currie, R. William. "Protein synthesis in perfused rat hearts after in vivo hyperthermia and in vitro cold ischemia." Biochemistry and Cell Biology 66, no. 1 (January 1, 1988): 13–19. http://dx.doi.org/10.1139/o88-002.

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Isolated and perfused rat hearts can be maintained for up to 2.5 h with minimal synthesis of a stress protein with a relative mass (Mr) of 71 kilodaltons (SP71). Isolated hearts, subjected to 17 h of cold (4 °C) ischemia, upon perfusion (37 °C) synthesize a large amount of SP71. In the present study, the effect of in vivo hyperthermia on protein synthesis in isolated and perfused hearts was examined. Hearts were excised from rats subjected to a 15-min episode of hyperthermia (42 °C), either immediately (no recovery) or after 24 h of recovery. The excised hearts were perfused either immediately or after 17 h of cold ischemia. Hyperthermia (no recovery) increased [3H]leucine incorporation into SP71, while hyperthermia with a 24-h recovery did not increase incorporation into SP71 during perfusion (no ischemia). Hyperthermia (no recovery) increased the incorporation of [3H]leucine into SP71 seen after cold ischemia. Hyperthermia with a 24-h recovery decreased the incorporation of [3H]leucine into SP71 seen after cold ischemia. This reduction in synthesis of SP71 after 24-h recovery from hyperthermia could be caused by the accumulation of SP71 suppressing its own synthesis or a measure of protection (tolerance) induced by the hyperthermia.

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Evteev, V. A., R. E. Kazakov, A. B. Prokof'ev, I. A. Mazerkina, and N. D. Bunyatyan. "Activity of renal organic anion transporters in a model of ischemia and reperfusion injury in vitro." Sechenov Medical Journal, no. 4 (December 30, 2018): 25–27. http://dx.doi.org/10.47093/22187332.2018.4.25-27.

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The aim of the work is to study the functional characteristics of SLC transporters of organic anions: OAT1 and OAT3 in normal conditions and in model ischemia/reperfusion injury.Materials and methods. The HEK293 cell line was used as a model for the study. Conditions of ischemia/reperfusion injury were created by the previously described method. The activity of the transporters was assessed by the capture of the marker substrate - ﬂuorescein. The concentration of ﬂuorescein was measured using a plate ﬂuorimeter. The results were normalized by the amount of total protein.Results. In condition of ischemia/reperfusion injury, the activity of organic anion transporters decreased in comparison with the norm. The data obtained allow us to conclude that in conditions of ischemia/reperfusion injury, the concentration of dicarboxylic acids in the cell is low, which in turn can lead to a decrease activity of transporters.

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Steenbergen, C., M. L. Hill, and R. B. Jennings. "Cytoskeletal damage during myocardial ischemia: changes in vinculin immunofluorescence staining during total in vitro ischemia in canine heart." Circulation Research 60, no. 4 (April 1987): 478–86. http://dx.doi.org/10.1161/01.res.60.4.478.

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Adachi, Naoto, Junfeng Chen, Keyue Liu, Shinzo Tsubota, and Tatsuru Arai. "Dexamethasone Aggravates Ischemia-Induced Neuronal Damage by Facilitating the Onset of Anoxic Depolarization and the Increase in the Intracellular Ca2+ Concentration in Gerbil Hippocampus." Journal of Cerebral Blood Flow & Metabolism 18, no. 3 (March 1998): 274–80. http://dx.doi.org/10.1097/00004647-199803000-00005.

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The Ca2+ mobilization across the neuronal membrane is regarded as a crucial factor in the development of neuronal damage in ischemia. Because glucocorticoids have been reported to aggravate ischemic neuronal injury, the effects of dexamethasone on ischemia-induced membrane depolarization, histologic outcome, and changes in the intracellular Ca2+ concentration in the gerbil hippocampus were examined in vivo and in vitro. The effects of metyrapone, an inhibitor of glucocorticoid synthesis, were also evaluated. Changes in the direct-current potential shift in the hippocampal CA1 area produced by transient forebrain ischemia for 2.5 minutes were compared among animals pretreated with dexamethasone (3 μg, intracerebroventricularly), metyrapone (100 mg/kg, intraperitoneally), and saline. The histologic outcome was evaluated 7 days after ischemia by assessing the delayed neuronal death in the hippocampal CA1 pyramidal cells of these animals. A hypoxia-induced intracellular Ca2+ increase was evaluated by in vitro microfluorometry in gerbil hippocampal slices, and the effect of dexamethasone (120 μg/L in the medium) on the cytosolic Ca2+ accumulation was examined. The effect in a Ca2+-free ischemialike condition was also investigated. Preischemic administration of dexamethasone reduced the onset latency of ischemia-induced membrane depolarization by 22%, and aggravated neuronal damage in vivo. In contrast, pretreatment with metyrapone improved the histologic outcome. The onset time of the increase in the intracellular concentration of Ca2+ provoked by in vitro hypoxia was advanced in dexamethasone-treated slices. The Ca2+-free in vitro hypoxia reduced the elevation compared with that in the Ca2+-containing condition. Treatment with dexamethasone facilitated the increase on both the initiation and the extent in the Ca2+-free condition. Aggravation of ischemic neuronal injury by endogenous or exogenous glucocorticoids is thus thought to be caused by the advanced onset times of both the ischemia-induced direct-current potential shift and the increase in the intracellular Ca2+ concentration.

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MacGregor, Duncan G., Marat V. Avshalumov, and Margaret E. Rice. "Brain edema induced by in vitro ischemia: causal factors and neuroprotection." Journal of Neurochemistry 85, no. 6 (May 13, 2003): 1402–11. http://dx.doi.org/10.1046/j.1471-4159.2003.01772.x.

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Jung, Keun-Hwa, Kon Chu, Soon-Tae Lee, Lami Kang, Seung U. Kim, Manho Kim, and Jae-Kyu Roh. "G-CSF protects human cerebral hybrid neurons against in vitro ischemia." Neuroscience Letters 394, no. 3 (February 2006): 168–73. http://dx.doi.org/10.1016/j.neulet.2005.10.040.

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32

Mittmann, T., M. Qü, K. Zilles, and H. J. Luhmann. "Long-term cellular dysfunction after focal cerebral ischemia: in vitro analyses." Neuroscience 85, no. 1 (March 1998): 15–27. http://dx.doi.org/10.1016/s0306-4522(97)00638-6.

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33

Gabryel, Bożena, Jakub Adamczyk, Małgorzata Huzarska, Anna Pudełko, and Henryk I. Trzeciak. "Aniracetam Attenuates Apoptosis of Astrocytes Subjected to Simulated Ischemia In Vitro." NeuroToxicology 23, no. 3 (September 2002): 385–95. http://dx.doi.org/10.1016/s0161-813x(02)00084-0.

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34

Sinor, Amy D., Stacy M. Irvin, and David A. Greenberg. "Endocannabinoids protect cerebral cortical neurons from in vitro ischemia in rats." Neuroscience Letters 278, no. 3 (January 2000): 157–60. http://dx.doi.org/10.1016/s0304-3940(99)00922-2.

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35

Tomori, H., M. Shiraishi, H. Koga, M. Toure, K. Taira, T. Higa, Y. Okuhama, S. Hiroyasu, and Y. Muto. "Protective effects of lidocaine in hepatic ischemia/reperfusion injury in vitro." Transplantation Proceedings 30, no. 7 (November 1998): 3740–42. http://dx.doi.org/10.1016/s0041-1345(98)01217-2.

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36

Jiang, W., F. Fu, J. Tian, H. Zhu, and J. Hou. "Curculigoside A attenuates experimental cerebral ischemia injury in vitro and vivo." Neuroscience 192 (September 2011): 572–79. http://dx.doi.org/10.1016/j.neuroscience.2011.06.079.

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37

Li, Yachen, Yongming Bao, Bo Jiang, Zhuo Wang, Yuxin Liu, Cen Zhang, and Lijia An. "Catalpol protects primary cultured astrocytes from in vitro ischemia‐induced damage." International Journal of Developmental Neuroscience 26, no. 3-4 (January 31, 2008): 309–17. http://dx.doi.org/10.1016/j.ijdevneu.2008.01.006.

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38

Roque, Cláudio, and Graça Baltazar. "Impact of Astrocytes on the Injury Induced by In Vitro Ischemia." Cellular and Molecular Neurobiology 37, no. 8 (March 17, 2017): 1521–28. http://dx.doi.org/10.1007/s10571-017-0483-3.

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39

Mdzinarishvili, A., C. Kiewert, V. Kumar, M. Hillert, and J. Klein. "Bilobalide prevents ischemia-induced edema formation in vitro and in vivo." Neuroscience 144, no. 1 (January 2007): 217–22. http://dx.doi.org/10.1016/j.neuroscience.2006.08.037.

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40

Gao, Q., Y. Li, L. Shen, J. Zhang, X. Zheng, R. Qu, Z. Liu, and M. Chopp. "Bone marrow stromal cells reduce ischemia-induced astrocytic activation in vitro." Neuroscience 152, no. 3 (March 2008): 646–55. http://dx.doi.org/10.1016/j.neuroscience.2007.10.069.

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41

Bagó, Marcell, Dénes B. Horváthy, Melinda Simon, Bence Marschall, Ana Pinto, Olga Kuten, Dora Polsek, István Hornyák, Stefan Nehrer, and Zsombor Lacza. "Temperature controlled dual hypoxic chamber design for in vitro ischemia experiments." Biocybernetics and Biomedical Engineering 38, no. 3 (2018): 498–503. http://dx.doi.org/10.1016/j.bbe.2018.03.010.

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42

Casiraghi, Monica, Jason R. Tatreau, John B. Abano, John W. Blackwell, Larry Watson, Keith Burridge, Scott H. Randell, and Thomas M. Egan. "In vitro modeling of nonhypoxic cold ischemia–reperfusion simulating lung transplantation." Journal of Thoracic and Cardiovascular Surgery 138, no. 3 (September 2009): 760–67. http://dx.doi.org/10.1016/j.jtcvs.2009.05.037.

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43

Jin, K. L., X. O. Mao, and D. A. Greenberg. "Vascular endothelial growth factor: Direct neuroprotective effect in in vitro ischemia." Proceedings of the National Academy of Sciences 97, no. 18 (August 29, 2000): 10242–47. http://dx.doi.org/10.1073/pnas.97.18.10242.

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44

Towfigh, Shirin, Tracy Heisler, David A. Rigberg, O. Joe Hines, Jason Chu, David W. McFadden, and Charles Chandler. "Intestinal Ischemia and the Gut–Liver Axis: An in Vitro Model." Journal of Surgical Research 88, no. 2 (February 2000): 160–64. http://dx.doi.org/10.1006/jsre.1999.5767.

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45

Zhan, Ren-Zhi, Naoshi Fujiwara, Hiroshi Endoh, Tomohiro Yamakura, Kiichiro Taga, Satoru Fukuda, and Koki Shimoji. "Thiopental Inhibits Increases in [Ca2+]iInduced by Membrane Depolarization, NMDA Receptor Activation, and Ischemia in Rat Hippocampal and Cortical Slices." Anesthesiology 89, no. 2 (August 1, 1998): 456–66. http://dx.doi.org/10.1097/00000542-199808000-00023.

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Background This study examined the effects of thiopental on intracellular calcium ([Ca2+]i) changes induced by membrane depolarization, N-methyl-D-aspartate (NMDA) receptor activation, and ischemia. Methods Experiments were performed in brain slices prepared from Wistar rats. [Ca2+]i measurements were taken on the CA1 pyramidal cell layer of the hippocampus or layers II to III of the somatosensory cortex using the fura-2 fluorescence technique. Membrane depolarization and NMDA receptor activation were induced by exposing slices to 60 mM K+ and 100 microM NMDA, respectively. In vitro ischemia was induced by superfusing slices with glucose-free Krebs solution equilibrated with 95% nitrogen and 5% carbon dioxide. Thiopental was applied 5 min before application of high K+ and NMDA, or before in vitro ischemia. Results Ischemia for 15 min produced a characteristic [Ca2+]i increase in both hippocampal and cortical slices. Thiopental prolonged the latency to the appearance of the [Ca2+]i plateau and reduced the magnitudes of increase in [Ca2+]i 8, 10, and 15 min after the onset of ischemia. Thiopental also suppressed the high K+- and NMDA-induced [Ca2+]i increases. The NMDA-induced [Ca2+]i increases were attenuated to a greater extent in cortical slices than were those in hippocampal slices. The inhibition of thiopental on the 200-microM NMDA-mediated [Ca2+]i response was confirmed in cultured cortical neurons. Conclusions The results indicate that thiopental attenuates ischemia-induced [Ca2+]i increases in the hippocampus and cortex in vitro, probably because of its inhibition of both voltage-gated calcium channels and NMDA receptors. The regionally different inhibition of thiopental on NMDA receptors may relate to its region-specific action against ischemia.

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46

Zhou, An, Manabu Minami, Xiaoman Zhu, Sylvia Bae, John Minthorne, Jingquan Lan, Zhi-gang Xiong, and Roger P. Simon. "Altered Biosynthesis of Neuropeptide Processing Enzyme Carboxypeptidase E after Brain Ischemia: Molecular Mechanism and Implication." Journal of Cerebral Blood Flow & Metabolism 24, no. 6 (June 2004): 612–22. http://dx.doi.org/10.1097/01.wcb.0000118959.03453.17.

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In this study, using both in vivo and in vitro ischemia models, the authors investigated the impact of brain ischemia on the biosynthesis of a key neuropeptide-processing enzyme, carboxypeptidase E (CPE). The response to brain ischemia of animals that lacked an active CPE was also examined. Combined in situ hybridization and immunocytochemical analyses for CPE showed reciprocal changes of CPE mRNA and protein, respectively, in the same cortical cells in rat brains after focal cerebral ischemia. Western blot analysis revealed an accumulation of the precursor protein of CPE in the ischemic cortex in vivo and in ischemic cortical neurons in vitro. Detailed metabolic labeling experiments on ischemic cortical neurons showed that ischemic stress caused a blockade in the proteolytic processing of CPE. When mice lacking an active CPE protease were subjected to a sublethal episode of focal cerebral ischemia, abundant TUNEL-positive cells were seen in the ischemic cortex whereas only a few were seen in the cortex of wild-type animals. These findings suggest that ischemia has an adverse impact on the neuropeptide-processing system in the brain and that the lack of an active neuropeptide-processing enzyme exacerbates ischemic brain injury.

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47

Popovic, Robert, Richard Liniger, and Philip E. Bickler. "Anesthetics and Mild Hypothermia Similarly Prevent Hippocampal Neuron Death in an In Vitro Model of Cerebral Ischemia." Anesthesiology 92, no. 5 (May 1, 2000): 1343–49. http://dx.doi.org/10.1097/00000542-200005000-00024.

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Background General anesthetics reduce neuron loss following focal cerebral ischemia in rodents. The relative efficacy of this action among different anesthetics clinically used for neuroprotection is uncertain. In addition, it remains unclear how anesthetics compare to neuroprotection afforded by mild hypothermia. This study was performed to evaluate the comparative effects of isoflurane, sodium pentothal, and mild hypothermia in a hippocampal slice model of cerebral ischemia and to determine if the mechanism of neuroprotection of isoflurane involves inhibition of glutamate excitotoxicity. Methods Survival and morphology of CA1, CA3, and dentate gyrus neurons in rat hippocampal slices were examined after 10 or 20 min of combined oxygen-glucose deprivation (in vitro ischemia) followed by a 5-h recovery period. Results 10 or 20 min in vitro ischemia at 37 degrees C killed 35-40% of neurons in CA1 (P < 0.001), 6% in CA3 (not significant) and 18% in dentate (P < 0.05). Isoflurane (0.7 and 2.0%, approximately 0.45 and 1.5 minimum alveolar concentration), pentothal (50 microm, approximately 1 minimum alveolar concentration equivalent) and mild hypothermia (34 degrees C) all reduced CA1 cell loss and morphologic damage to similar degrees in 10- and 20-min periods of ischemia (P < 0.001). The noncompetitive N-methyl-D-aspartate antagonist MK-801 prevented cell damage, showing that N-methyl-D-aspartate receptor activation is an important mechanism of injury in this model. Glutamate (1 mm) produced cell loss similar to in vitro ischemia. Isoflurane (2%) prevented cell damage from glutamate exposure. Conclusions In hippocampal slices, neuron death from simulated ischemia was predominately due to activation of glutamate receptors. Isoflurane, sodium pentothal, an N-methyl-D-aspartate receptor antagonist, and mild hypothermia prevented cell death to similar degrees. For isoflurane, the mechanism appears to involve attenuation of glutamate excitotoxicity.

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48

Ling, Chengli, Chang Lei, Manshu Zou, Xiong Cai, Yun Xiang, Yu Xie, Xuran Li, Dan Huang, and Yuhong Wang. "Neuroprotective effect of apigenin against cerebral ischemia/reperfusion injury." Journal of International Medical Research 48, no. 9 (September 2020): 030006052094585. http://dx.doi.org/10.1177/0300060520945859.

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Objective The therapeutic efficacy of apigenin in PC12 cells and rats remains uncertain. The aim of this study was to investigate the neuroprotective effects of apigenin against cerebral ischemia/reperfusion injury, both in vitro and in vivo. Methods We first treated PC12 cells with cobalt chloride (CoCl2) to create a model of oxidative stress injury. Cell viability was then determined using a multifunctional microplate reader. In addition, reactive oxygen species (ROS) levels, apoptosis, and mitochondrial membrane potentials (MMPs) were examined using high-content cytometer analysis. The efficacy of apigenin treatment was also analyzed in a rat middle cerebral artery occlusion (MCAO) model using TTC staining and neurological deficit scores. Results The half-inhibitory concentration of CoCl2 was 1.2 mM. Pretreatment with 10 µg ⋅ mL−1 apigenin significantly enhanced cell viability, reduced ROS levels, alleviated apoptosis, and improved MMP in PC12 cells with CoCl2-induced injury in vitro. In addition, apigenin treatment in vivo significantly improved neurological deficit scores and reduced infarct areas in MCAO rats. These results suggest that the neuroprotective mechanisms of apigenin may be related to mitochondrial activation. Conclusions Apigenin had excellent neuroprotective effects for the treatment of cerebral ischemia/reperfusion injury in vitro and in vivo.

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Alechinsky, Louise, Frederic Favreau, Petra Cechova, Sofiane Inal, Pierre-Antoine Faye, Cecile Ory, Raphaël Thuillier, et al. "Tannic Acid Improves Renal Function Recovery after Renal Warm Ischemia–Reperfusion in a Rat Model." Biomolecules 10, no. 3 (March 12, 2020): 439. http://dx.doi.org/10.3390/biom10030439.

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Background and purpose: Ischemia–reperfusion injury is encountered in numerous processes such as cardiovascular diseases or kidney transplantation; however, the latter involves cold ischemia, different from the warm ischemia found in vascular surgery by arterial clamping. The nature and the intensity of the processes induced by ischemia types are different, hence the therapeutic strategy should be adapted. Herein, we investigated the protective role of tannic acid, a natural polyphenol in a rat model reproducing both renal warm ischemia and kidney allotransplantation. The follow-up was done after 1 week. Experimental approach: To characterize the effect of tannic acid, an in vitro model of endothelial cells subjected to hypoxia–reoxygenation was used. Key results: Tannic acid statistically improved recovery after warm ischemia but not after cold ischemia. In kidneys biopsies, 3 h after warm ischemia–reperfusion, oxidative stress development was limited by tannic acid and the production of reactive oxygen species was inhibited, potentially through Nuclear Factor erythroid-2-Related factor 2 (NRF2) activation. In vitro, tannic acid and its derivatives limited cytotoxicity and the generation of reactive oxygen species. Molecular dynamics simulations showed that tannic acid efficiently interacts with biological membranes, allowing efficient lipid oxidation inhibition. Tannic acid also promoted endothelial cell migration and proliferation during hypoxia. Conclusions: Tannic acid was able to improve renal recovery after renal warm ischemia with an antioxidant effect putatively extended by the production of its derivatives in the body and promoted cell regeneration during hypoxia. This suggests that the mechanisms induced by warm and cold ischemia are different and require specific therapeutic strategies.

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Cybulsky, Andrey V., Tomoko Takano, Julie Guillemette, Joan Papillon, Rildo A. Volpini, and John A. Di Battista. "The Ste20-like kinase SLK promotes p53 transactivation and apoptosis." American Journal of Physiology-Renal Physiology 297, no. 4 (October 2009): F971—F980. http://dx.doi.org/10.1152/ajprenal.00294.2009.

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Expression and activity of the germinal center SLK are increased during kidney development and recovery from renal ischemia-reperfusion injury. SLK promotes apoptosis, in part, via pathway(s) involving apoptosis signal-regulating kinase-1 and p38 mitogen-activated protein kinase. This study addresses the role of p53 as a potential effector of SLK. p53 transactivation was measured after transient transfection of a luciferase reporter plasmid that contains a p53 cis-acting enhancer element. Overexpression of SLK in COS-1 cells and cotransfection of SLK and p53-wild type (wt) cDNAs in glomerular epithelial cells (GECs) stimulated p53 transactivational activity, as measured by a p53 response element-driven luciferase reporter. In GECs, chemical anoxia followed by glucose reexposure (in vitro ischemia-reperfusion) increased p53 reporter activity, and this increase was amplified by overexpression of SLK. Expression of SLK induced p53 phosphorylation on serine (S)-33 and S315. In GECs, cotransfection of SLK with p53-wt, p53-S33A, p53-S315A, or p53-S33A+S315A mutants showed that only the double mutation abolished the SLK-induced increase in p53 reporter activity. SLK-induced stimulation of p53 reporter activity was attenuated by inhibition of JNK. Overexpression of SLK amplified apoptosis induced by subjecting cells to in vitro ischemia-reperfusion injury, while ectopic expression of a dominant negative SLK mutant attenuated the ischemia-reperfusion-induced apoptosis. The p53 transactivation inhibitor pifithrin-α significantly attenuated the amount of apoptosis after ischemia-reperfusion and SLK overexpression. Thus SLK induces p53 phosphorylation and transactivation, which enhances apoptosis after in vitro ischemia-reperfusion injury.

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