Analyzing the anti-ischemia-reperfusion injury effects of ginsenoside Rb1 mediated through the inhibition of p38α MAPK.

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 p38α 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-α) in the myocardium were monitored. The expressions of p38α MAPK, caspase-3, and TNF-α in the myocardium were assayed. GS Rb1 reduced MIS and attenuated caspase-3 activity and the levels of TNF-α in the myocardium. Protein expression of total p38α MAPK was not significantly altered. In the Ani + I/R and I/R groups, the levels of phospho-p38α 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 p38α MAPK phosphorylation, suggesting that GS Rb1-mediated protection requires the inhibition of p38α MAPK.

• Authors: Gonghao Li, Wenhao Qian, Changyun Zhao
• Journal: Canadian journal of physiology and pharmacology (Can J Physiol Pharmacol) Vol. 94 Issue 1 Pg. 97-103 (Jan 2016) ISSN: 1205-7541 [Electronic] Canada
• PMID: 26550918 (Publication Type: Journal Article)

Chemical References

• Cardiotonic Agents
• Ginsenosides
• Imidazoles
• Protein Kinase Inhibitors
• Pyridines
• Tumor Necrosis Factor-alpha
• ginsenoside Rb1
• Mitogen-Activated Protein Kinase 14
• Casp3 protein, rat
• Caspase 3
• SB 203580

Topics

• Animals
• Cardiotonic Agents (pharmacology)
• Caspase 3 (metabolism)
• Ginsenosides (pharmacology)
• Imidazoles (pharmacology)
• Male
• Mitogen-Activated Protein Kinase 14 (antagonists & inhibitors)
• Myocardial Infarction (pathology, prevention & control)
• Myocardial Reperfusion Injury (enzymology, physiopathology, prevention & control)
• Phosphorylation (drug effects)
• Protein Kinase Inhibitors (pharmacology)
• Pyridines (pharmacology)
• Rats
• Rats, Sprague-Dawley
• Tumor Necrosis Factor-alpha (metabolism)