Analyzing The Anti-Ischemia-Reperfusion Injury Effects Of Ginsenoside Rb1 Mediated Through The Inhibition Of P38 Alpha Mapk
CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY(2016)
Abstract
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.
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Key words
ginsenoside Rb1, myocardial ischemia-reperfusion injury, apoptosis, P38 alpha MAPK, SB203580
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