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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Analyzing the anti-ischemia-reperfusion injury effects of ginsenoside Rb1 mediated through the inhibition of p38 alpha MAPK
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Analyzing the anti-ischemia-reperfusion injury effects of ginsenoside Rb1 mediated through the inhibition of p38 alpha MAPK

机译：分析人参皂苷Rb1通过抑制p38αMAPK介导的抗缺血再灌注损伤作用

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摘要

Recent studies have demonstrated that ginsenoside Rb1 protects the myocardium from ischemia-reperfusion (I/R) injury. However, the precise mechanisms for this protection have not been determined. This study aimed to determine whether the attenuation of I/R-induced myocardial injury by ginsenoside Rb1 (GS Rb1) is due to inhibition of p38 alpha mitogen-activated protein kinase (MAPK). Sprague-Dawley rats were distributed among 6 treatment groups: sham group; I/R group; p38 MAPK inhibitor SB203580 group (SB + I/R); GS Rb1 group (GS + I/R); p38 MAPK agonist anisomycin group (Ani + I/R); and the GS Rb1 + Ani group (GS + Ani + I/R). All of the anaesthetized rats, except those in the sham group, underwent an open-chest procedure that involved 30 min of myocardial ischemia followed by 2 h of reperfusion. Myocardial infarction size (MIS), caspase-3 activity, and levels of the cytokine tumor necrosis factor alpha (TNF-alpha) in the myocardium were monitored. The expressions of p38 alpha MAPK, caspase-3, and TNF-alpha in the myocardium were assayed. GS Rb1 reduced MIS and attenuated caspase-3 activity and the levels of TNF-alpha in the myocardium. Protein expression of total p38 alpha MAPK was not significantly altered. In the Ani + I/R and I/R groups, the levels of phospho-p38 alpha MAPK were significantly increased compared with the sham group, and these increased levels were reduced with GS Rb1. Hemodynamic parameters were not significantly different between the GS + I/R and SB + I/R groups. GS Rb1 exerts an anti-apoptotic effect that protects against I/R injury by inhibiting p38 alpha MAPK phosphorylation, suggesting that GS Rb1-mediated protection requires the inhibition of p38 alpha MAPK.
机译：最近的研究表明，人参皂甙Rb1保护心肌免受缺血再灌注（I / R）损伤。但是，尚未确定用于这种保护的确切机制。这项研究旨在确定人参皂甙Rb1（GS Rb1）对I / R诱导的心肌损伤的减轻是否是由于抑制了p38α促分裂原活化蛋白激酶（MAPK）。 Sprague-Dawley大鼠分为6个治疗组：假手术组;假手术组;假手术组。 I / R组; p38 MAPK抑制剂SB203580组（SB + I / R）; GS Rb1组（GS + I / R）; p38 MAPK激动剂茴香霉素组（Ani + I / R）;以及GS Rb1 + Ani组（GS + Ani + I / R）。除假手术组外，所有麻醉大鼠均进行开胸手术，涉及30分钟的心肌缺血，然后再灌注2小时。监测心肌梗死面积（MIS），caspase-3活性和心肌细胞因子肿瘤坏死因子α（TNF-alpha）的水平。测定了p38αMAPK，caspase-3和TNF-α在心肌中的表达。 GS Rb1降低了MIS，并减弱了caspase-3活性和心肌中TNF-α的水平。总p38αMAPK的蛋白表达没有明显改变。与假手术组相比，在Ani + I / R和I / R组中，磷酸化p38αMAPK的水平显着增加，而GS Rb1则降低了这些增加的水平。 GS + I / R和SB + I / R组之间的血流动力学参数无显着差异。 GS Rb1发挥抗凋亡作用，可通过抑制p38αMAPK磷酸化来防止I / R损伤，这表明GS Rb1介导的保护作用需要抑制p38αMAPK。

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