scholarly journals Cardioprotective Effect of K-7259, a Novel Dilazep Derivative, against Ischemia-Reperfusion Damage in Isolated, Working Rat Hearts.

1997 ◽  
Vol 73 (4) ◽  
pp. 365-369 ◽  
Author(s):  
A.N. Ehsanul Hoque ◽  
Nina Hoque ◽  
Akiyoshi Hara ◽  
Hiroko Hashizume ◽  
Kazuo Ichihara ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
Cardioprotective Effect ◽  
Reperfusion Damage ◽  
Rat Hearts

scholarly journals Cardioprotective Effect of K-7259, a Novel Dilazep Derivative, against Ischemia-Reperfusion Damage in Isolated, Working Rat Hearts

1997 ◽  
Vol 73 (4) ◽  
pp. 365-369
Author(s):  
A.N. Ehsanul Hoque ◽  
Nina Hoque ◽  
Akiyoshi Hara ◽  
Hiroko Hashizume ◽  
Kazuo Ichihara ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
Cardioprotective Effect ◽  
Reperfusion Damage ◽  
Rat Hearts

scholarly journals Dexmedetomidine Protects against Myocardial Ischemia/Reperfusion Injury by Ameliorating Oxidative Stress and Cell Apoptosis through the Trx1-Dependent Akt Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Zhi-lin Wu ◽  
Jacques Robert Jeppe Davis ◽  
Yi Zhu
Keyword(s):  
Oxidative Stress ◽  
Myocardial Ischemia ◽  
Cardiac Function ◽  
Cell Apoptosis ◽  
Ischemia Reperfusion ◽  
Cardioprotective Effect ◽  
Akt Pathway ◽  
Rat Hearts ◽  
Myocardial Ischemia Reperfusion ◽  
Isolated Rat

Dexmedetomidine (Dex) was reported to reduce oxidative stress and protect against myocardial Ischemia/Reperfusion (I/R) injury. However, the molecular mechanism involved in its antioxidant property is not fully elucidated. The present study was aimed at investigating whether the Trx1/Akt pathway participated in the cardioprotective effect of Dex. In the present study, I/R-induced myocardial injury in isolated rat hearts and OGD/R-induced injury in H9c2 cardiomyocytes were established. Our findings suggested that Dex ameliorated myocardial I/R injury by improving cardiac function, reducing myocardial apoptosis and oxidative stress, which was manifested by increased GSH and SOD contents, decreased ROS level, and MDA generation in both the isolated rat hearts and OGD/R-treated H9C2 cells. More importantly, it was found that the level of Trx1 was preserved, and Akt phosphorylation was significantly upregulated by Dex treatment. However, these effects of Dex were abolished by PX-12 (a specific Trx1 inhibitor) administration. Taken together, this study suggests that Dex plays a protective role in myocardial I/R injury, improves cardiac function, and relieves oxidative stress and cell apoptosis. Furthermore, our results present a novel signaling mechanism that the cardioprotective effect of Dex is at least partly achieved through the Trx1-dependent Akt pathway.

scholarly journals Fisetin Attenuates Myocardial Ischemia-Reperfusion Injury by Activating the Reperfusion Injury Salvage Kinase (RISK) Signaling Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Karthi Shanmugam ◽  
Sri Rahavi Boovarahan ◽  
Priyanka Prem ◽  
Bhavana Sivakumar ◽  
Gino A Kurian
Keyword(s):  
Oxidative Stress ◽  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Signaling Pathway ◽  
Isolated Heart ◽  
Ischemia Reperfusion ◽  
Cardioprotective Effect ◽  
Myocardial Infarct Size ◽  
Myocardial Oxidative Stress ◽  
Rat Hearts

Ischemia-reperfusion (I/R) injury is an unavoidable injury that occurs during revascularization procedures. In the previous study, we reported that fisetin is a natural flavonoid that attenuates I/R injury by suppressing mitochondrial oxidative stress and mitochondrial dysfunction. Though fisetin is reported as a GSK3β inhibitor, it remains unclear whether it attenuates myocardial ischemia by activating the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) pathway, thereby inhibiting the downstream GSK3β, or by directly interacting with GSK3β while rendering its cardioprotection. In this study, the research team investigates the possible mechanism of action of fisetin while rendering its cardioprotective effect against myocardial I/R injury in rats. For this investigation, the team utilized two myocardial I/R models: Ligation of the left anterior descending artery and Langendorff isolated heart perfusion system. The latter has no neurohormonal influences. The PI3K inhibitor (Wortmannin, 0.015 mg/kg), GSK3β inhibitor (SB216763, 0.7 mg/kg), and fisetin (20 mg/kg) were administered intraperitoneally before inducing myocardial I/R. The result of this study reveals that the administration of fisetin decreases the myocardial infarct size, apoptosis, lactate dehydrogenase, and creatine kinase in serum\perfusate of the rat hearts subjected to I/R. However, the inhibition of PI3K with Wortmannin significantly reduced the cardioprotective effect of fisetin both in the ex vivo and vivo models. The administration of GSK3β inhibitor after the administration of fisetin and Wortmannin, re-establishing the cardioprotection, indicates the major role of PI3K in fisetin action. Changes in myocardial oxidative stress (level) and mitochondrial functional preservation of interfibrillar and subsarcolemmal mitochondria support the above findings. Hence, the team here reports that fisetin conferred its cardioprotection against I/R injury by activating the PI3K/Akt/GSK3β signaling pathway in rat hearts.

Cardioprotective properties of citicoline against hyperthyroidism-induced reperfusion damage in rat hearts

2015 ◽  
Vol 93 (3) ◽  
pp. 185-191 ◽  
Author(s):  
Luz Hernández-Esquivel ◽  
Natalia Pavón ◽  
Mabel Buelna-Chontal ◽  
Héctor González-Pacheco ◽  
Javier Belmont ◽  
...  
Keyword(s):  
Body Weight ◽  
Protective Effect ◽  
Ventricular Arrhythmias ◽  
Inhibitory Action ◽  
Ischemia Reperfusion ◽  
Permeability Transition ◽  
Electrical Behavior ◽  
Reperfusion Damage ◽  
Rat Hearts ◽  
Increased Risk

Hyperthyroidism represents an increased risk factor for cardiovascular morbidity, especially when the heart is subjected to an ischemia/reperfusion process. The aim of this study was to explore the possible protective effect of the nucleotide citicoline on the susceptibility of hyperthyroid rat hearts to undergo reperfusion-induced damage, which is associated with mitochondrial dysfunction. Hence, we analyzed the protective effect of citicoline on the electrical behavior and on the mitochondrial function in rat hearts. Hyperthyroidism was established after a daily i.p. injection of triiodothyronine (at 2 mg/kg of body weight) during 5 days. Thereafter, citicoline was administered i.p. (at 125 mg/kg of body weight) for 5 days. In hyperthyroid rat hearts, citicoline protected against reperfusion-induced ventricular arrhythmias. Moreover, citicoline maintained the accumulation of mitochondrial Ca2+, allowing mitochondria to reach a high transmembrane electric gradient that protected against the release of cytochrome c. It also preserved the activity of the enzyme aconitase that inhibited the release of cytokines. The protection also included the inhibition of oxidative stress-induced mDNA disruption. We conclude that citicoline protects against the reperfusion damage that is found in the hyperthyroid myocardium. This effect might be due to its inhibitory action on the permeability transition in mitochondria.

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