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10.1155/2018/9173436 http://scihub22266oqcxt.onion/10.1155/2018/9173436 C5845518!5845518 !29636855     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29636855 &cmd=llinks): Failed to open stream: HTTP request failed! 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Fisetin Confers Cardioprotection against Myocardial Ischemia Reperfusion Injury by Suppressing Mitochondrial Oxidative Stress and Mitochondrial Dysfunction and Inhibiting Glycogen Synthase Kinase 3? Activity |pdf=|usr=}}{{29636855 }} gab.com Text Fisetin Confers Cardioprotection against Myocardial Ischemia Reperfusion Injury by Suppressing Mitochondrial Oxidative Stress and Mitochondrial Dysfunction and Inhibiting Glycogen Synthase Kinase 3 Activity JO: Oxid Med Cell Longev http://www.kidney.de/pget.php?&tw=1&pmid=29636855 #FOAvip Acute myocardial infarction (AMI) is the leading cause of morbidity and mortality worldwide. Timely reperfusion is considered an optimal treatment for AMI. Paradoxically, the procedure of reperfusion can itself cause myocardial tissue injury. Therefore, a strategy to minimize the reperfusion-induced myocardial tissue injury is vital for salvaging the healthy myocardium. Herein, we investigated the cardioprotective effects of fisetin, a natural flavonoid, against ischemia/reperfusion (I/R) injury (IRI) using a Langendorff isolated heart perfusion system. I/R produced significant myocardial tissue injury, which was characterized by elevated levels of lactate dehydrogenase and creatine kinase in the perfusate and decreased indices of hemodynamic parameters. Furthermore, I/R resulted in elevated oxidative stress, uncoupling of the mitochondrial electron transport chain, increased mitochondrial swelling, a decrease of the mitochondrial membrane potential, and induction of apoptosis. Moreover, IRI was associated with a loss of the mitochondrial structure and decreased mitochondrial biogenesis. However, when the animals were pretreated with fisetin, it significantly attenuated the I/R-induced myocardial tissue injury, blunted the oxidative stress, and restored the structure and function of mitochondria. Mechanistically, the fisetin effects were found to be mediated via inhibition of glycogen synthase kinase 3? (GSK3?), which was confirmed by a biochemical assay and molecular docking studies. Twit Text FOAVip Fisetin Confers Cardioprotection against Myocardial Ischemia Reperfusion Injury by Suppressing Mitochondrial Oxidative Stress and Mitochondrial Dysfunction and Inhibiting Glycogen Synthase Kinase 3 Activity ????Oxid Med Cell Longev http://www.kidney.de/pget.php?&tw=1&pmid=29636855 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29636855 #FOAvip English Wikipedia <ref>{{Cite pmid|29636855 }}</ref> Fisetin Confers Cardioprotection against Myocardial Ischemia Reperfusion Injury by Suppressing Mitochondrial Oxidative Stress and Mitochondrial Dysfunction and Inhibiting Glycogen Synthase Kinase 3? Activity #MMPMID29636855 Shanmugam K ; Ravindran S ; Kurian GA ; Rajesh M Oxid Med Cell Longev 2018[]; 2018 (ä): 9173436 PMID29636855 show ga Acute myocardial infarction (AMI) is the leading cause of morbidity and mortality worldwide. Timely reperfusion is considered an optimal treatment for AMI. Paradoxically, the procedure of reperfusion can itself cause myocardial tissue injury. Therefore, a strategy to minimize the reperfusion-induced myocardial tissue injury is vital for salvaging the healthy myocardium. Herein, we investigated the cardioprotective effects of fisetin, a natural flavonoid, against ischemia/reperfusion (I/R) injury (IRI) using a Langendorff isolated heart perfusion system. I/R produced significant myocardial tissue injury, which was characterized by elevated levels of lactate dehydrogenase and creatine kinase in the perfusate and decreased indices of hemodynamic parameters. Furthermore, I/R resulted in elevated oxidative stress, uncoupling of the mitochondrial electron transport chain, increased mitochondrial swelling, a decrease of the mitochondrial membrane potential, and induction of apoptosis. Moreover, IRI was associated with a loss of the mitochondrial structure and decreased mitochondrial biogenesis. However, when the animals were pretreated with fisetin, it significantly attenuated the I/R-induced myocardial tissue injury, blunted the oxidative stress, and restored the structure and function of mitochondria. Mechanistically, the fisetin effects were found to be mediated via inhibition of glycogen synthase kinase 3? (GSK3?), which was confirmed by a biochemical assay and molecular docking studies. |Animals [MESH] |Flavonoids/pharmacology/*therapeutic use [MESH] |Flavonols [MESH] |Glycogen Synthase Kinase 3 beta/*antagonists & inhibitors [MESH] |Male [MESH] |Mitochondria/*metabolism [MESH] |Myocardial Infarction/*drug therapy/pathology [MESH] |Myocardial Reperfusion Injury/*drug therapy/pathology [MESH] |Oxidative Stress/*drug effects [MESH]Fisetin Confers Cardioprotection against Myocardial Ischemia Reperfusi(epmc).pdf DeepDyve Pubget Overpricing