title: 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.affiliation: a Institute of Cardiovascular Disease Research, Xuzhou Medical College, Xuzhou, Jiangsu, China.
authors.forename: Gonghao
authors.initials: G
authors.lastname: Li
authors.affiliation: b Department of Cardiology, Research Institute of Cardiovascular Disease, the Affiliated Hospital of Xuzhou Medical College, 84 West Huaihai Road, Xuzhou, Jiangsu 221002, China.
authors.forename: Wenhao
authors.initials: W
authors.lastname: Qian
authors.affiliation: a Institute of Cardiovascular Disease Research, Xuzhou Medical College, Xuzhou, Jiangsu, China.
authors.forename: Changyun
authors.initials: C
authors.lastname: Zhao
mesh_terms: D000818:Animals; D002316:Cardiotonic Agents / Q000494:pharmacology*; D053148:Caspase 3 / Q000378:metabolism; D036145:Ginsenosides / Q000494:pharmacology*; D007093:Imidazoles / Q000494:pharmacology; D008297:Male; D048308:Mitogen-Activated Protein Kinase 14 / Q000037:antagonists & inhibitors*; D009203:Myocardial Infarction / Q000473:pathology / Q000517:prevention & control; D015428:Myocardial Reperfusion Injury / Q000201:enzymology* / Q000503:physiopathology / Q000517:prevention & control*; D010766:Phosphorylation / Q000187:drug effects; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D011725:Pyridines / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D002316:Cardiotonic Agents; D036145:Ginsenosides; D007093:Imidazoles; D047428:Protein Kinase Inhibitors; D011725:Pyridines; D014409:Tumor Necrosis Factor-alpha; C442759:ginsenoside Rb1; D048308:Mitogen-Activated Protein Kinase 14; C505410:Casp3 protein, rat; D053148:Caspase 3; C093642:SB 203580
keywords: MAP kinase p38α; P38α MAPK; SB203580; apoptose; apoptosis; ginsenoside Rb1; ginsénoside Rb1; lésion d’ischémie–reperfusion myocardique; myocardial ischemia–reperfusion injury