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Abstract

Nuclear Role of LOX-1 in XinMaiJia-attenuating Atherosclerosis in Rabbits

Author(s): R. L. Sun, T. T. Zhu1, M. L. Zhu1, P. Song1, J. Xu1, Y. L. Yin2* and P. Li1*
Henan Key Laboratory of immunology and targeted therapy, Henan Collaborative Innovation Center of Molecular Diagnosis and Laboratory Medicine, School of Laboratory Medicine, 1College of Pharmacy, 2School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, Henan 453003, China

Correspondence Address:
College of Pharmacy, Xinxiang Medical University, Xinxiang, Henan 453003, China, E-mail: pengli@xxmu.edu.cn


This study aimed to explore the nuclear role of lectin-like oxidised low density lipoprotein receptor-1 in atherosclerotic rabbits treated with XinMaiJia to further confirm that low density lipoprotein receptor-1 is a target of XinMaiJia in attenuating atherosclerosis. Atherosclerotic model of rabbits was established. Lovastatin, zhibituo and different concentrations of XinMaiJia were administered to atherosclerotic rabbits. Pathological examination was performed on the right common carotid artery, cytokines reflected inflammation and oxidative stress level were detected. Moreover, endothelin-1, low density lipoprotein receptor-1 and endothelial nitric oxide synthase expression were measured. XinMaiJia prevented the development of atherosclerosis and reduced low density lipoprotein receptor-1 expression in rabbits. For antioxidant effect, XinMaiJia increased superoxide dismutase activity but decreased malondialdehyde level in plasma. For antiinflammation effect, XinMaiJia increased the expression of endothelial nitric oxide synthase and nitric oxide, but reduced intercellular adhesion molecule-1, vascular cell adhesion molecule-1, matrix metalloprotein-2 and nuclear factor-kappa B levels. Furthermore, XinMaiJia reduced endothelin-1 expression. More importantly, all these changes have a feedback with low density lipoprotein receptor-1. XinMaiJia increased the antioxidant and antiinflammation capacity of the body to prevent the development of atherosclerosis. The possible mechanisms of XinMaiJia were mainly through inhibiting the vital gene low density lipoprotein receptor-1.

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