Daming capsule restores endothelial dysfunction induced by high-fat diet
- Equal contributors
1 Department of Pharmacology, (the State-Province Key Laboratory of Biomedicine and Pharmaceutics), and Key Laboratory of Cardiovascular Research, Ministry of Education, Harbin 150086, Peoples' Republic of China
2 Department of Pathology, Harbin Medical University, Harbin 150081, Peoples' Republic of China
BMC Complementary and Alternative Medicine 2012, 12:21 doi:10.1186/1472-6882-12-21Published: 24 March 2012
Daming capsule (DMC), a traditional Chinese formula, has a lipid-modulating action with reduced adverse side effects as compared with other lipid lowering compounds. Since endothelial dysfunction often accompanies the hyperlipidemic state, we hypothesize that DMC might restore endothelial dysfunction produced by a high-fat (HF) diet. Importantly, we also investigate possible mechanisms involved in mediating the effects of DMC on vascular reactivity.
Rats were divided into four groups: control, HF diet, HF mixed DMC diet, HF mixed atorvastatin (ATV) diet. After 30 days, the thoracic cavity was exposed to remove the thoracic aorta for (i) histological examination; (ii) measurement of endothelial nitric oxide synthase (eNOS) by western blot; and (iii) tension study of thoracic aortic ring.
HF diet induced significant attenuation in the contraction and relaxation of rat aortic rings. Treatment with DMC significantly improved the relaxation of the aortic rings as compared with those from HF rats (P < 0.05), which was abolished by a nonspecific NOS inhibitor L-NAME. Moreover DMC significantly restored the decrease in eNOS expression induced by HF diet. Similar results were found in histopathologic changes. DMC failed to restore the loss of vasocontraction of aorta explained by an impairment of ATP-sensitive K+ channels (KATP) on the structure and/or function. DMC exerted the same protective effect as ATV, a positive control drug, on vascular injury produced by HF diet.
DMC partially protects the aorta from HF-induced endothelial dysfunction via upregulation of the expression of eNOS.