Daming capsule restores endothelial dysfunction induced by high-fat diet

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.Hyperlipidemia is an important independent risk factor for cardiovascular diseases. Hyperlipidemia is accompanied by vascular disease such as: atherosclerosis, angiostenosis and blocking, which may induce hypertension, cerebral apoplexy, myocardial infarction, and even sudden cardiac death. Accumulating evidence indicates that a high-fat diet induces both systemic and tissue oxidative stress and the development of early vascular lesions [1]. Impaired endothelial function, an early hallmark of atherogenesis, was observed in rats and healthy volunteers fed high-saturated fat and high-sucrose meals [2,3]. Moreover, nitric oxide (NO) produced by endothelium was inhibited by high-fat diet [4]. Hyperlipidemia and oxidation of low density lipoprotein (LDL) induce vascular smooth muscle cell growth [5] and hyperlipidemia may alter the vascular resp