The protective effect of quercetin on the vascular endothelial cells injured by homocysteine in rabbits / 中国药理学通报

AIM To observe the protective effect of quercetin on vascular endothelial cells injured by homocysteine in rabbits. METHODS The model of the vascular endothelial cells of rabbits injured by homocysteine was established; 50 mg?kg -1, 100 mg?kg -1 and 200 mg?kg -1 of quercetin were orally adminstered. After 30 days, the number of CEC, levels of MDA and NO,SOD activity in the serum were determined; ET concentration in the plasma was detected. The thoracic aorta was isolated to observe the vascular reactivity to nitroglycerin and ACh and tissue change. RESULTS The number of CEC, levels of MDA and ET were decreased and levels of SOD and NO were significantly increased in the quercetin-administered group compared with the injured group.Non-endothelium dependent relaxation of vessel caused by nitroglycerin was similar in all groups. Endothelium dependent relaxation caused by ACh was reduced in the injured group,whileas the relaxation trended to the normal degree in the quercetin-administered group. Pathological examination showed that quercetin was effective on the injured endothelial cells. CONCLUSION Quercetin produces protective effect on the injured vascular endothelial cells by homocysteine in rabbits.

New pathway of atherosclerotic drug therapy——anti-inflammatory effect / 中国药理学通报

There are increasing experimental evidences and clinical data showing that inflammatory reaction plays an important role in the production and development of atherosclerosis. Inflammatory process promotes the production and release of inflammatory factors by activation of monocytes and stimulation of endothelial cells, which stimulate the migration and proliferation of vascular smooth muscle cells. Hydrolases and cytokines are released from the activated and stimulated cells to increase local lesion and form atherosclerotic plaque with the development of inflammation. So, on the basis of the new pathogenesis of atherosclerosis,scientists try to interfere with atherosclerosis by anti-inflammatory pathway. This paper reviews the progress of drugs against atherosclerosis by the modulation of C reaction protein ,CD40-CD40L,infection and NF-?B.