Protective effect of Xin-Ji-Er-Kang on cardiovascular remodeling in high salt-induced hypertensive mice

Abstract

The aim of the present study was to investigate the effects of Xin-Ji-Er-Kang (XJEK) on high salt-induced hypertensive mice. Mice with high-salt diet-induced hypertension were divided into four groups: Control (standard diet alone for 8 weeks), model (diet containing 8% NaCl for 8 weeks and intragastric administration of distilled water for the last 4 weeks), XJEK + high-salt-treated (diet containing 8% NaCl for 8 weeks and intragastric administration of XJEK for the last 4 weeks) and irbesartan + high-salt-treated (diet containing 8% NaCl for 8 weeks with intragastric administration of irbesartan for the last 4 weeks). The hemodynamic index and cardiac pathological changes in the hypertensive mice were then examined. An aortic ring apparatus was used to detect acetylcholine-dependent endothelium relaxation function. Colorimetric analysis was applied to determine serum nitric oxide (NO), superoxide dismutase activity and malondialdehyde content; ELISA was employed to measure brain natriuretic peptide, serum angiotensin II (Ang II), endothelin-1 content and aldosterone; and immunohistochemistry was used to detect the expression of endothelial nitric oxide synthase (eNOS), interleukin (IL)-1β, IL-10 and tumor necrosis factor (TNF)-α in cardiac tissues. XJEK improved the heart systolic and diastolic function, ameliorated hemodynamic parameters and cardiovascular remodeling indices, blunted the cardiac pathological changes and improved endothelial dysfunction (ED) via boosting eNOS activity, promoting NO bioavailability and decreasing serum Ang II content. Furthermore, treatment with XJEK inhibited the increase of IL-1β and TNF-α expression and the decrease of IL-10 expression in cardiac tissues, and ameliorated oxidative stress status. Therefore, XJEK exerted protective effects against high salt-induced hypertension and cardiovascular remodeling in mice via improving ED, restoring pro- and anti-inflammatory factor balance and decreasing oxidative stress.