In this study, the cardioprotective mechanism of the combination of notoginseng total saponins and safflower total flavonoids(CNS) was investigated due to its excellently efficacy against myocardial infarction(MI)...In this study, the cardioprotective mechanism of the combination of notoginseng total saponins and safflower total flavonoids(CNS) was investigated due to its excellently efficacy against myocardial infarction(MI) in rats. After the left anterior descending coronary artery(LADCA) ligation, rats were orally administered with CNS for 7 consecutive days. CNS prevented MI-induced pathophysiological changes and significantly decreased plasma levels of myocardial enzymes, including creatine kinase MB isoenzyme(CK-MB), lactate dehydrogenase(LDH) and aspartate aminotransferase(AST). Further investigation revealed that CNS attenuated the production of inflammatory factors in plasma, including tumor necrosis factor-alpha(TNF-α), interleukin-6(IL-6) and interleukin-1β(IL-1β). Moreover, CNS treatment decreased the expression of caspase-3 at the mR NA level in infarct tissue. Our findings demonstrated that the anti-inflammatory and anti-apoptotic properties of CNS might confer its cardioprotection against MI in rats.展开更多
基金National Natural Sciences Foundation of China(Grant No.81573684)
文摘In this study, the cardioprotective mechanism of the combination of notoginseng total saponins and safflower total flavonoids(CNS) was investigated due to its excellently efficacy against myocardial infarction(MI) in rats. After the left anterior descending coronary artery(LADCA) ligation, rats were orally administered with CNS for 7 consecutive days. CNS prevented MI-induced pathophysiological changes and significantly decreased plasma levels of myocardial enzymes, including creatine kinase MB isoenzyme(CK-MB), lactate dehydrogenase(LDH) and aspartate aminotransferase(AST). Further investigation revealed that CNS attenuated the production of inflammatory factors in plasma, including tumor necrosis factor-alpha(TNF-α), interleukin-6(IL-6) and interleukin-1β(IL-1β). Moreover, CNS treatment decreased the expression of caspase-3 at the mR NA level in infarct tissue. Our findings demonstrated that the anti-inflammatory and anti-apoptotic properties of CNS might confer its cardioprotection against MI in rats.