Semen cassiae extract attenuates myocardial ischemia and reperfusion injury in type 2 diabetic rats
- VernacularTitle:决明子提取物减轻2型糖尿病大鼠心肌缺血/再灌注损伤
- Author:
Libing LIU
;
Haifeng ZHANG
- Publication Type:Journal Article
- Keywords:
semen cassiae;
diabetes;
myocardial ischemia/reperfusion injury;
Akt;
ERK1/2
- From:
Basic & Clinical Medicine
2015;(1):1-6
- CountryChina
- Language:Chinese
-
Abstract:
Objective Obese patients with type 2 diabetes mellitus ( T2DM) characterized by hyperglycemia are li-able to more severe myocardial infarction .Semen Cassiae is proved to reduce serum lipid level .This study was to investigate whether the Semen Cassiae extract (SCE) reduces myocardial ischemia and reperfusion (MI/R) injury with or without diabetes and the underlying mechanisms .Methods The high-fat diet-fed streptozotocin ( HFD-STZ) rat model was used as T2DM model.Normal and DM rats received SCE treatment orally (10 mg/kg/day) for 1 week.Subsequently these animals were subjected to MI /R.Results Compared with the normal animals , DM rats showed increased plasma total cholesterol ( TC) and triacylglycerol ( TG) , more severe MI/R injury and cardi-ac functional impairment .SCE treatment significantly reduced the plasma TC and TG , improved the instantaneous first derivation of left ventricle pressure and reduced infarct size , decreased plasma creatine kinase and lactate dehydrogenase levels, and reduced apoptosis index at the end of reperfusion in diabetic rats .Moreover, SCE treat-ment increased the antiapoptotic protein Akt and stimulated ERK 1/2 phosphorylation .Pretreatment with a PI3 K in-hibitor wortmannin or an ERK1/2 inhibitor PD98059 not only blocked Akt and ERK1/2 phosphorylation, but also inhibited the cardioprotective effects of SCE .However , SCE treatment did not show any effects on the MI/R injury in the normal rats.Conclusions SCE effectively improves myocardial function and reduces MI/R-induced injury in diabetic but not normal animals , which is potentially attributable to the reduced TC/TG levels and the triggered cell survival signaling Akt and ERK 1/2 .