Effect of Xin Mai Jia on atherosclerosis in rats

• Published in: Genetics and molecular research Vol. 14; no. 2; pp. 6018 - 6027
• Main Authors: Li, P, Pan, G P, Jia, M, Wang, Q Q, Guo, Z G, Zhao, F R, Lei, G L, Wan, G R, Wan, G M
• Format: Journal Article
• Language: English
• Published: Brazil 01.06.2015
• Subjects: Angiotensins - biosynthesis; Angiotensins - blood; Animals; Atherosclerosis - blood; Atherosclerosis - chemically induced; Atherosclerosis - drug therapy; Cholesterol - blood; Diet, High-Fat; Endothelin-1 - biosynthesis; Endothelin-1 - blood; Endothelium, Vascular - metabolism; Endothelium, Vascular - pathology; Gene Expression; Humans; Lipoproteins, LDL - blood; Male; Medicine, Chinese Traditional; Nitric Oxide - metabolism; Nitric Oxide Synthase Type III - biosynthesis; Nitric Oxide Synthase Type III - blood; Rats; Vitamin D - toxicity
• ISSN: 1676-5680; 1676-5680
• DOI: 10.4238/2015.June.1.19

We investigated the therapeutic effect of Xin Mai Jia (XMJ) on atherosclerosis (AS) in rats. Rat models of AS were established by peritoneally injecting vitamin D, feeding a high-fat diet, and inducing balloon injuries in rats. The stomachs of the rats were irrigated continuously for 10 weeks with XMJ. Blood lipid- and hemorheology-related indices of blood samples were detected. Pathological changes in the right common carotid arterial tissues were also determined. The protein expression levels of endothelial nitric oxide synthase, angio-tensin-1, and endothelin-1 were determined by western blotting. XMJ reduced cholesterol, trigylecride, and low-density lipoprotein levels as well as blood viscosity, sedimentation, and hematocrit. Furthermore, XMJ alleviated vascular endothelial injury and reduced/eliminated atherosclerotic plaques. In contrast, XMJ significantly increased the endothelium-dependent relaxing response of the AS rat models. The western blotting results showed that XMJ upregulated endothelial nitric oxide synthase but downregulated angiotensin-1 and endothelin-1. XMJ prevented the development of AS by regulating blood lipid levels, hemorheology, and vascular function.