Jujuboside A Ameliorates Myocardial Apoptosis and Inflammation in Rats with Coronary Heart Disease by Inhibiting PPAR-α Signaling Pathway.

Background. Coronary heart disease (CHD) is a chronic disease caused by atherosclerosis (AS), which can cause myocardial ischemia, hypoxia, or necrosis, seriously threatening human health. There is an urgent need for effective treatments and drugs to reduce the various risk factors for coronary heart disease and relieve symptoms of angina pectoris and myocardial infarction in patients. Jujuboside A (JuA) is a triterpenoid saponin extracted from jujube seeds, which has various biological activities such as antioxidant, anti-inflammatory, antiapoptotic, and neuroprotective effects. We study the function of JuA in myocardial injury, dyslipidemia, and inflammation in the CHD rat model, to explore its potential mechanism of improving CHD. Methods. A rat model of CHD was established by feeding a high-fat diet. The rats were randomly divided into 5 groups (n = 6): control group, CHD group, JuA 25 mg/kg group, JuA 50 mg/kg group, and JuA 75 mg/kg group. Echocardiography was used to detect the cardiac function parameters of rats in each group, and then, hematoxylin and eosin staining was used to assess the histopathological injury in myocardial tissues. Levels of blood lipids, myocardial injury indexes, and inflammatory factors of rats in each group were measured by biochemical tests and enzyme linked immunosorbent assay, and the levels of Bax, Bcl-2, c-caspase-3, PPAR-α, p65, p-p65, IκBα, and p-IκBα protein expression in myocardial tissues were detected by western blot. Results. Compared with the CHD group, JuA therapy significantly improved injury in myocardial tissue and endothelial tissue. It also strengthened cardiac function, while decreasing total cholesterol, triacylglycerol, and low-density lipoprotein cholesterol levels in the serum and increasing high-density lipoprotein cholesterol levels. In addition, JuA also restrained cardiomyocytes apoptosis and inhibited the inflammatory reaction by reducing TNF-α, IL-1β, and IL-6 expression in myocardial tissues. Furthermore, administration of JuA inhibited the activation of PPAR-α pathway by preventing the phosphorylation of p65 and IκBα in myocardial tissues of CHD rats. Conclusion. JuA may improve cardiac function, alleviate myocardial and endothelial injury, and also ameliorate dyslipidemia and inflammatory reaction in rats with CHD, where JuA probably plays a protective role by inhibiting the activation of PPAR-α pathway. [ABSTRACT FROM AUTHOR]

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