Salvianolic Acid B Protects Against Myocardial Ischemia-reperfusion Injury In Rats Via Inhibiting The Expression Of High Mobility Group Box 1 Protein Through

ObjectiveThe aim of this study was to determine the effects of Sal B in myocardial ischemia-reperfusion(I/R)injury in rats and to explore its underlying mechanism of cardioprotection whether through activating the expression of the phosphoinositide 3-kinase/protein,kinase B(PI3K/Akt)and inhibitting the expression of high mobility group protein 1(HMGB1).MethodsNinety sprague-dawley(SD)rats were randomized into the five groups.Sham-operated group(Sham),myocardial I/R group(I/R),low dose of Sal B+I/R group(Sal-L),high dose of Sal B+I/R group(Sal-H),High dose of Sal B+I/R+LY294002 group(Sal-H-LY),LY294002:a specific PI3k inhibitor.All I/R groups received 30 min myocardial ischemia followed by 24 h reperfusion.ResultsCompared with the sham-operated group,echocardiography showed that the values of cardiac output(CO)and left ventricular ejection fraction(EF)decreased significantly(P<0.05)and the area of infarct in I/R group rats was larger in I/R group(P<0.05),L-lactate dehydrogenase(L-LDH),creatine kinase isoenzyme(CK-MB),tumor necrosis factor-α(TNF-α),interleukin-18(IL-18),interleukin-1β(IL-1β),high mobility group box-1 protein(HMGB1)and immunohistochemical detection of HMGB1,Toll-like receptor 4(TLR4)in the I/R group were significantly higher.The level of phosphorylated protein kinase B(P-Akt)protein decreased significantly(P<0.05).Compared with the model group,Sal B increased the values of EF and CO,reduced myocardial infarction size in a dose-dependent manner(P<0.05),decreased the levels of L-LDH,CK-MB,TNF-α,IL-18,IL-1β and HMGB1(P<0.05),activated PI3K/Akt signaling pathway,and inhibited the expression of HMGB1 and TLR4 proteins(P<0.05).However,LY294002 significantly reversed the therapeutic effect of SalB(P<0.05).ConclusionSal B protects against myocardial I/R injury in rats via inhibiting the expression of HMGB1 protein through PI3K/Akt signaling pathway.