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Articles de revues sur le sujet « Modello ischemia in vitro »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 31 juillet 2025

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1

Visocchi, M., M. Meglio, D. Cabezas Cuevas, et al. "Sensibilità e specificità della RM in un nuovo modello di ictus ischemico acuto sperimentale «collaterale»." Rivista di Neuroradiologia 9, no. 1 (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'is

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Pelliccioli, G. P., P. F. Ottaviano, C. Gambelunghe, et al. "Ischemia cerebrale sperimentale nei gerbillo." Rivista di Neuroradiologia 6, no. 3 (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

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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 (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 ischem

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

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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 (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

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

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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 (2009): 421–29. http://dx.doi.org/10.1007/s12272-009-1316-9.

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Ye, Zhouheng, Bradley P. Ander, Frank R. Sharp та Xinhua Zhan. "Cleaved β-Actin May Contribute to DNA Fragmentation Following Very Brief Focal Cerebral Ischemia". Journal of Neuropathology & Experimental Neurology 77, № 3 (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

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Hoebart, Clara, Attila Kiss, Bruno K. Podesser, Ammar Tahir, Michael J. M. Fischer, and Stefan Heber. "Sensory Neurons Release Cardioprotective Factors in an In Vitro Ischemia Model." Biomedicines 12, no. 8 (2024): 1856. http://dx.doi.org/10.3390/biomedicines12081856.

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Sensory neurons densely innervate the myocardium. The role of their sensing and response to acute and prolonged ischemia is largely unclear. In a cellular model of ischemia-reperfusion injury, the presence of sensory neurons increases cardiomyocyte survival. Here, after the exclusion of classical neurotransmitter release, and measurement of cytokine release, we modified the experiment from a direct co-culture of primary murine cardiomyocytes and sensory neurons to a transfer of the supernatant. Sensory neurons were exposed to ischemia and the resulting conditioned supernatant was transferred o

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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 (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 co

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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 (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, lact

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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 (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

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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 (2011): 1241–52. http://dx.doi.org/10.1038/labinvest.2011.79.

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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 (2010): 20–27. http://dx.doi.org/10.1016/j.jneumeth.2010.04.017.

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

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

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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 (1986): 785–93. http://dx.doi.org/10.1016/0301-5629(86)90076-1.

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Schurr, Avital, Ralphiel S. Payne, Kenneth H. Reid, et al. "Cardiac arrest-induced global cerebral ischemia studied in vitro." Life Sciences 57, no. 26 (1995): 2425–30. http://dx.doi.org/10.1016/0024-3205(95)02238-7.

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Zhan, Ren-Zhi, Naoshi Fujiwara, Hiroshi Endoh, et al. "Thiopental Inhibits Increases in [Ca2+]iInduced by Membrane Depolarization, NMDA Receptor Activation, and Ischemia in Rat Hippocampal and Cortical Slices." Anesthesiology 89, no. 2 (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 w

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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 (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 expr

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Zhou, An, Manabu Minami, Xiaoman Zhu, et al. "Altered Biosynthesis of Neuropeptide Processing Enzyme Carboxypeptidase E after Brain Ischemia: Molecular Mechanism and Implication." Journal of Cerebral Blood Flow & Metabolism 24, no. 6 (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 corte

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Shin, Tae Hwan, Da Yeon Lee, Shaherin Basith, et al. "Metabolome Changes in Cerebral Ischemia." Cells 9, no. 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 protein

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Alechinsky, Louise, Frederic Favreau, Petra Cechova, et al. "Tannic Acid Improves Renal Function Recovery after Renal Warm Ischemia–Reperfusion in a Rat Model." Biomolecules 10, no. 3 (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 af

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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 (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

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Perez-Pinzon, M. A., L. Tao, and C. Nicholson. "Extracellular potassium, volume fraction, and tortuosity in rat hippocampal CA1, CA3, and cortical slices during ischemia." Journal of Neurophysiology 74, no. 2 (1995): 565–73. http://dx.doi.org/10.1152/jn.1995.74.2.565.

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1. An in vitro slice model of ischemia was used to study changes in extracellular potassium concentration and diffusion properties in the stratum pyramidale of CA1 and CA3 regions of the hippocampus and in the cortex of the rat. Slices were submerged in artificial cerebrospinal fluid, and ischemia was induced by removing oxygen and glucose until anoxic depolarization occurred. 2. Extracellular potassium concentration was measured with a valinomycin-based ion-selective microelectrode. The bathing medium contained 5 mM potassium, and in vitro ischemia caused the potassium concentration to rise t

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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 (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. Met

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Hu, Qingsong, Gen Suzuki, Rebeccah F. Young, Brian J. Page, James A. Fallavollita, and John M. Canty. "Reductions in mitochondrial O2 consumption and preservation of high-energy phosphate levels after simulated ischemia in chronic hibernating myocardium." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 1 (2009): H223—H232. http://dx.doi.org/10.1152/ajpheart.00992.2008.

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We performed the present study to determine whether hibernating myocardium is chronically protected from ischemia. Myocardial tissue was rapidly excised from hibernating left anterior descending coronary regions (systolic wall thickening = 2.8 ± 0.2 vs. 5.4 ± 0.3 mm in remote myocardium), and high-energy phosphates were quantified by HPLC during simulated ischemia in vitro (37°C). At baseline, ATP (20.1 ± 1.0 vs. 26.7 ± 2.1 μmol/g dry wt, P < 0.05), ADP (8.1 ± 0.4 vs. 10.3 ± 0.8 μmol/g, P < 0.05), and total adenine nucleotides (31.2 ± 1.3 vs. 40.1 ± 2.9 μmol/g, P < 0.05) were depresse

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Hadley, Gina, Ain A. Neuhaus, Yvonne Couch, et al. "The role of the endoplasmic reticulum stress response following cerebral ischemia." International Journal of Stroke 13, no. 4 (2017): 379–90. http://dx.doi.org/10.1177/1747493017724584.

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Background Cornu ammonis 3 (CA3) hippocampal neurons are resistant to global ischemia, whereas cornu ammonis (CA1) 1 neurons are vulnerable. Hamartin expression in CA3 neurons mediates this endogenous resistance via productive autophagy. Neurons lacking hamartin demonstrate exacerbated endoplasmic reticulum stress and increased cell death. We investigated endoplasmic reticulum stress responses in CA1 and CA3 regions following global cerebral ischemia, and whether pharmacological modulation of endoplasmic reticulum stress or autophagy altered neuronal viability . Methods In vivo: male Wistar ra

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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 (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 ty

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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 (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

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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 o

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Zheng, Shuai, Wenjing Li, Mingjiang Xu, et al. "Calcitonin gene-related peptide promotes angiogenesis via AMP-activated protein kinase." American Journal of Physiology-Cell Physiology 299, no. 6 (2010): C1485—C1492. http://dx.doi.org/10.1152/ajpcell.00173.2010.

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Ischemia induces angiogenesis as a compensatory response. Although ischemia is known to causes synthesis and release of calcitonin gene-related peptide (CGRP), it is not clear whether CGRP regulates angiogenesis under ischemia and how does it function. Thus we investigated the role of CGRP in angiogenesis and the involved mechanisms. We found that CGRP level was increased in the rat hindlimb ischemic tissue. The expression of exogenous CGRP by adenovirus vectors enhanced blood flow recovery and increased capillary density in ischemic hindlimbs. In vitro, CGRP promoted human umbilical vein endo

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Dong, Lingjun, Fuxiang Liang, Zhiling Lou, et al. "Necrostatin-1 Alleviates Lung Ischemia-Reperfusion Injury via Inhibiting Necroptosis and Apoptosis of Lung Epithelial Cells." Cells 11, no. 19 (2022): 3139. http://dx.doi.org/10.3390/cells11193139.

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Lung ischemia-reperfusion injury (LIRI) is associated with many diseases, including primary graft dysfunction after lung transplantation, and has no specific and effective therapies. Necroptosis contributes to the pathogenesis of ischemia-reperfusion injury. Necrostatin-1 (Nec-1), the necroptosis inhibitor targeting RIPK1, has been reported to alleviate ischemia-reperfusion injury in various organs. However, the underlying mechanism of Nec-1 in LIRI remains unclear. In this paper, an in vivo LIRI model was built up by left lung hilar clamping in mice, and an in vitro cold ischemia-reperfusion

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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 (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 sever

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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 (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

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Han, Moon-Ku, Manho Kim, So Yon Bae, et al. "VEGF protects human cerebral hybrid neurons from in vitro ischemia." NeuroReport 15, no. 5 (2004): 847–50. http://dx.doi.org/10.1097/00001756-200404090-00022.

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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 (2007): 143–59. http://dx.doi.org/10.1016/j.yexmp.2007.03.002.

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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 (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 grea

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

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Tang, Larissa Ho Ching, Frederic Khe Cheong Fung, Angela Ka Wai Lai, Ian Yat Hin Wong, Kendrick Co Shih, and Amy Cheuk Yin Lo. "Autophagic Upregulation Is Cytoprotective in Ischemia/Reperfusion-Injured Retina and Retinal Progenitor Cells." International Journal of Molecular Sciences 22, no. 16 (2021): 8446. http://dx.doi.org/10.3390/ijms22168446.

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The cytoprotective versus cytotoxic role of macroautophagy in ocular ischemia/reperfusion injuries remains controversial and its effects under hyperglycemia are unclear. We investigated the involvement of autophagy in in vitro and in vivo normoglycemic and hyperglycemic models of retinal ischemia/reperfusion injury. Retinal ischemia (2 h) and reperfusion (2 or 22 h) was induced in wild-type and type I diabetic Ins2Akita/+ mice using a middle cerebral artery occlusion model. R28 retinal precursor cells were subjected to CoCl2-induced hypoxia with or without autophagic inhibitor NH4Cl. Autophagi

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Burda, Jozef, M. Elena Martín, Miroslav Gottlieb та ін. "The Intraischemic and Early Reperfusion Changes of Protein Synthesis in the Rat Brain. eIF-2α Kinase Activity and Role of Initiation Factors eIF-2α and eIF-4E". Journal of Cerebral Blood Flow & Metabolism 18, № 1 (1998): 59–66. http://dx.doi.org/10.1097/00004647-199801000-00006.

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Rats were subjected to the standard four-vessel occlusion model of transient cerebral ischemia (vertebral and carotid arteries). The effects of normothermic ischemia (37°C) followed or not by 30-minute reperfusion, as well as 30-minute postdecapitative ischemia, on translational rates were examined. Protein synthesis rate, as measured in a cell-free system, was significantly inhibited in ischemic rats, and the extent of inhibition strongly depended on duration and temperature, and less on the model of ischemia used. The ability of reinitiation in vitro (by using aurintricarboxylic acid) decrea

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Ling, Chengli, Chang Lei, Manshu Zou, et al. "Neuroprotective effect of apigenin against cerebral ischemia/reperfusion injury." Journal of International Medical Research 48, no. 9 (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 effi

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Liu, Yanwei, Xinning Wu, Deyong Du, et al. "p53 Inhibition Provides a Pivotal Protective Effect against Cerebral Ischemia-Reperfusion Injury via the Wnt Signaling Pathway." Cerebrovascular Diseases 50, no. 6 (2021): 682–90. http://dx.doi.org/10.1159/000516889.

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<b><i>Introduction:</i></b> Cerebral ischemia-reperfusion injury enhances brain injury and increases its morbidity and mortality. The purpose of our study was to further explore the specific pathogenesis of cerebral ischemia disease by studying the role of p53 in cerebral ischemia-reperfusion injury and its mechanism to provide a new target for the treatment of cerebral ischemia. <b><i>Methods:</i></b> Middle cerebral artery occlusion (MCAo) was established in rats. The changes in p53 and apoptotic proteins in the rat model were detected by quant

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Slatova, L. N., T. A. Fedorina, and E. P. Shatunova. "Experimental models of myocardial ischemia: classical approaches and innovations (review)." Siberian Journal of Clinical and Experimental Medicine 39, no. 1 (2024): 18–27. http://dx.doi.org/10.29001/2073-8552-2024-39-1-18-27.

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Myocardial ischemia is the basis for many acute and chronic conditions with great social significance. Therefore, experimental models that describe ischemia development in humans are necessary for a better understanding of the pathophysiology of these conditions and the development of medical and surgical methods of treatment.Aim: To compare current approaches to experimental modeling of myocardial ischemia considering the pathogenetic features of the simulated processes. The manuscript describes the main experimental models of myocardial ischemia: in vitro cellular models, ex vivo isolated he

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Chazelas, Pauline, Clara Steichen, Frédéric Favreau, et al. "Oxidative Stress Evaluation in Ischemia Reperfusion Models: Characteristics, Limits and Perspectives." International Journal of Molecular Sciences 22, no. 5 (2021): 2366. http://dx.doi.org/10.3390/ijms22052366.

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Ischemia reperfusion injury is a complex process consisting of a seemingly chaotic but actually organized and compartmentalized shutdown of cell function, of which oxidative stress is a key component. Studying oxidative stress, which results in an imbalance between reactive oxygen species (ROS) production and antioxidant defense activity, is a multi-faceted issue, particularly considering the double function of ROS, assuming roles as physiological intracellular signals and as mediators of cellular component damage. Herein, we propose a comprehensive overview of the tools available to explore o

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Packard, Amy E. B., Jason C. Hedges, Frances R. Bahjat, et al. "Poly-IC Preconditioning Protects against Cerebral and Renal Ischemia-Reperfusion Injury." Journal of Cerebral Blood Flow & Metabolism 32, no. 2 (2011): 242–47. http://dx.doi.org/10.1038/jcbfm.2011.160.

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Preconditioning induces ischemic tolerance, which confers robust protection against ischemic damage. We show marked protection with polyinosinic polycytidylic acid (poly-IC) preconditioning in three models of murine ischemia-reperfusion injury. Poly-IC preconditioning induced protection against ischemia modeled in vitro in brain cortical cells and in vivo in models of brain ischemia and renal ischemia. Further, unlike other Toll-like receptor (TLR) ligands, which generally induce significant inflammatory responses, poly-IC elicits only modest systemic inflammation. Results show that poly-IC is

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Jiang, Wenjiao, and Kun Hao. "Protective Action of Betulinic Acid on Cerebral Ischemia/Reperfusion Injury through Inflammation and Energy Metabolic Homeostasis." Applied Sciences 10, no. 7 (2020): 2578. http://dx.doi.org/10.3390/app10072578.

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This work evaluated the protective effects of betulinic acid (BA) in vitro cerebral ischemia/reperfusion and provides clues about its pharmacological mechanism. A rat model of middle cerebral artery occlusion (MCAO) was established to investigate the effects of BA on cerebral ischemia. SHSY5Y cell injury was induced by oxygen–glucose deprivation and recovery (OGD/R) to further verify the action of BA in vitro. Our data show a significant improvement in infarct size, neurological score, and cerebral edema after BA treatment. Enzyme linked immunosorbent assay (ELISA) data show that BA inhibited

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Blondeau, Nicolas, Inger Lauritzen, Catherine Widmann, Michel Lazdunski, and Catherine Heurteaux. "A Potent Protective Role of Lysophospholipids against Global Cerebral Ischemia and Glutamate Excitotoxicity in Neuronal Cultures." Journal of Cerebral Blood Flow & Metabolism 22, no. 7 (2002): 821–34. http://dx.doi.org/10.1097/00004647-200207000-00007.

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Lysophospholipids (LPLs) are important intermediates in the synthesis and degradation of membrane phospholipids. Here we show that certain LPLs, particularly lysophosphatidylcholine and lysophosphatidylinositol, prevent neuronal death both in an in vivo model of transient global ischemia and in an in vitro model of excitotoxicity using primary cultures of cerebellar granule cells exposed to high extracellular concentrations of glutamate (20–40 μmol/L). The intravenous injection of lysophosphatidylcholine or lysophosphatidylinositol at a concentration of 200 nmol/kg induced a survival of CA1 py

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Pilipović, Kristina, Anja Harej Hrkać, Natalia Kučić, and Jasenka Mršić-Pelčić. "Modeling Central Nervous System Injury In Vitro: Current Status and Promising Future Strategies." Biomedicines 11, no. 1 (2022): 94. http://dx.doi.org/10.3390/biomedicines11010094.

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The central nervous system (CNS) injury, which occurs because of mechanical trauma or ischemia/hypoxia, is one of the main causes of mortality and morbidity in the modern society. Until know, despite the fact that numerous preclinical and clinical studies have been undertaken, no significant neuroprotective strategies have been discovered that could be used in the brain trauma or ischemia treatment. Although there are many potential explanations for the failure of those studies, it is clear that there are questions regarding the use of experimental models, both in vivo and in vitro, when study

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Cho, Sunghee, Eun-Mi Park, Yoonseong Kim, et al. "Early c-Fos Induction after Cerebral Ischemia: A Possible Neuroprotective Role." Journal of Cerebral Blood Flow & Metabolism 21, no. 5 (2001): 550–56. http://dx.doi.org/10.1097/00004647-200105000-00009.

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The role of c-Fos in neurodegeneration or neuroprotection after cerebral ischemia is controversial. To investigate whether early c-Fos induction after ischemia is associated with neuroprotection, rats were subjected to 10 minutes of transient forebrain ischemia and c-Fos expression was examined. Resistant dentate granule cells and neurons in CA2–4 displayed more robust immunoreactivity than vulnerable neurons in the CA1 region of hippocampus during early hours of reperfusion. By 6 hours after reperfusion, c-Fos immunoreactivity was greatly diminished in all areas of the hippocampus. Administra

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