WANG Ying,LI Cai,ZHU Feng, et al. The effect of calcium dobesilate on the formation of atherosclerotic plaques and its mechanism[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2020, 50(5): 387-390.
Abstract：Objective: To discuss the effect of calcium dobesilate on the formation of atherosclerotic plaques in rabbits and its mechanism. Methods: Atherosclerotic plaque model was set up by liquid nitrogen frostbite in 24 health male New Zealand rabbits. The rabbits were randomly divided as the model group (n=12) and the treatment group (n=12). The model group was given high-fat diet for 8 weeks, while the treatment group was given high-fat diet and calcium dobesilate (0.15 mg·g-1·d-1) for 8 weeks. Serum endothelin-1 (ET-1), nitric oxide (NO) and vascular endothelial growth factor (VEGF) were measured by ELISA before the experiment and after 8 weeks of treatment. After 8 weeks, the animals were killed, the right common carotid artery was removed, and the pathomorphological changes were observed by light microscope and electron microscope. The expression of matrix metalloproteinase 9 (MMP-9) and plasminogen activator inhibitor-1 (PAI-1) were detected by immunohistochemistry. Results: After 8 weeks, the vascular intima in the model group showed typical atherosclerotic plaque lesions, while the vascular intima in the treatment group showed slight atherosclerotic plaque lesions. The expression of PAI-1 and MMP-9 protein was observed locally in the carotid arteries of both groups, but the expression level in the treatment group was significantly lower than that in the model group (P<0.05). The expression of ET-1 was significantly decreased. The expression of NO and VEGF was significantly increased in both groups, but the decrease in ET-1 in the treatment group was greater than that in the model group, the increase in NO and VEGF was greater than that in the model group, with significant difference (P<0.05). Conclusion: Calcium dobesilate can improve endothelial dysfunction by reducing the expression of PAI-1 and MMP-9 proteins in local vascular walls, reducing the ET-1 content in blood circulation and increasing the levels of NO and VEGF, which play the role of anti-atherosclerotic plaque formation.
