scholarly journals Cardioprotective effect of isorhamnetin against myocardial ischemia reperfusion (I/R) injury in isolated rat heart through attenuation of apoptosis

2020 ◽  
Vol 24 (11) ◽  
pp. 6253-6262 ◽  
Author(s):  
Yan Xu ◽  
Chun Tang ◽  
Shengyu Tan ◽  
Juan Duan ◽  
Hongmei Tian ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Rat Heart ◽  
Ischemia Reperfusion ◽  
Isolated Rat Heart ◽  
Cardioprotective Effect ◽  
Myocardial Ischemia Reperfusion ◽  
Isolated Rat

scholarly journals Cardioprotective Effects of Astragalin against Myocardial Ischemia/Reperfusion Injury in Isolated Rat Heart

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Daoxu Qu ◽  
Jichun Han ◽  
Huanhuan Ren ◽  
Wenxiao Yang ◽  
Xinjie Zhang ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Rat Heart ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Isolated Rat Heart ◽  
Sprague Dawley ◽  
Sod Activity ◽  
Cardioprotective Effects ◽  
Myocardial Ischemia Reperfusion ◽  
Isolated Rat

This study aims to evaluate the cardioprotective effects of astragalin against myocardial ischemia/reperfusion (I/R) injury in isolated rat heart. The cardioprotective effects of astragalin on myocardial I/R injury were investigated on Langendorff apparatus. Adult male Sprague-Dawley rats were randomly divided into five groups. The results showed that astragalin pretreatment improved myocardial function. Compared with I/R group, lactate dehydrogenase (LDH) and creatine kinase (CK) activities in coronary flow decreased in astragalin pretreatment groups, whereas superoxide dismutase (SOD) activity and glutathione/glutathione disulfide (GSH/GSSG) ratio significantly increased. The levels of malondialdehyde (MDA), intracellular reactive oxygen species (ROS), tumor necrosis factor-α(TNF-α), and interleukin-6 (IL-6) decreased in astragalin-treated groups. The infarct size (IS) and apoptosis rate in hearts from astragalin-treated groups were lower than those in hearts from the I/R group. Western blot analysis also revealed that astragalin preconditioning significantly reduced Bax level, whereas Bcl-2 was increased in the myocardium. Therefore, astragalin exhibited cardioprotective effects via its antioxidative, antiapoptotic, and anti-inflammatory activities.

scholarly journals Protective Effects ofElaeagnus angustifoliaLeaf Extract against Myocardial Ischemia/Reperfusion Injury in Isolated Rat Heart

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Binsheng Wang ◽  
Hengyi Qu ◽  
Jun Ma ◽  
Xiling Sun ◽  
Dong Wang ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Aqueous Extract ◽  
Rat Heart ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Isolated Rat Heart ◽  
Protective Effects ◽  
Elaeagnus Angustifolia ◽  
Myocardial Ischemia Reperfusion ◽  
Isolated Rat

The purpose of this study is to clarify the cardioprotective property of the aqueous extract ofElaeagnus angustifoliaL. leaf (EA) against myocardial ischemia/reperfusion injury in isolated rat heart. The myocardial ischemia/reperfusion (I/R) injury model of isolated rat heart was set up by the use of improved Langendorff retrograde perfusion technology. Compared with the ischemia/reperfusion (I/R) group, the aqueous extract ofElaeagnus angustifoliaL. leaf (0.5 mg/mL, 1.0 mg/mL) pretreatment markedly improved the coronary flow (CF) and raised left ventricular developed pressure (LVDP) and maximum rise/down velocity (±dp/dtmax). The infarct size of the EA-treated hearts was smaller than that of I/R group. After treatment with EA, the superoxide dismutase (SOD) activity increased; malondialdehyde (MDA) and protein carbonyl content reduced more obviously (P<0.01) than that of I/R injury myocardial tissue.Conclusion. Results from the present study showed that the aqueous extract ofElaeagnus angustifoliaL. leaf has obvious protective effects on myocardial I/R injury, which may be related to the improvement of myocardial oxidative stress states.

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.

Sign in / Sign up

Export Citation Format

Share Document