Effect Of Baicalin On Atherosclerosis And Adiponectin Level In Mice

Background:In recent years, the morbidity of atherosclerosis (AS) in the world were increase higher and gradually younger, it a serious threat to human health. AS is a long-term, complex,multi-factor process.lt is widely accepted that AS is a chronic inflammation of various factors on arterial endothelial damage resulted in the artery wall. More and more study find that adipokines play a very important role in the arising and development of AS, and adiponectin as an adipokine secreted by fat cell, the long-term epidemiological studies discovered that the low levels of adiponectin is a risk factor of AS. Adiponectin has anti-inflammation, ameliorating lipid metabolism, insulin sensitization,protection of endothelia fuction and anti-atherosclerosis.It plays an important protective effect in the development of chronic inflammatory process of AS.Baicalin is the major effective ingredient of radix scutellariae,and its main effectiveness includes powerful anti-inflammation, anti-tumor, anti-atheroscloresis, protecting liver, as well as its pharmacological effects includes improving endothelial function, resisting oxidative-stress induced damage in cells, restraining VSMCs proliferation, resisting atherosclerosis etc. This study explores the intervention of baicalin in atherosclerosis and the influence of baicalin on adiponectin expression, which provides a new theoretical foundation for the prevention and treatment of the atherosclerosis.Objective:Through feeding ApoE gene knoct mice to establish the model of atherosclerosis. Observe the expression levels of lipids, inflammatory cytokines, serum adiponectin, ICAM-1、VCAM-1and NF-κ B in atherosclerosis.To investigate the effects of baicalin on the atherosclerosis and adiponectin. Methods:10male C57BL/61mouse were control group and fed with normal diet.30male mice with ApoE deficiency(ApoE-/-) were divided randomly into As model group(n=10), baicalin high dose group(n=10) and baicalin low dose group(n=10) and the last three group fed with hypercholesterol diet. After12weeks, the baicalin high dose group were give bacalin50mg· kg-1· d-1, baicalin low dose group treated with bacalin25mg· kg-1· d-1.The normal group and AS model group treated physiological saline lml/d. Serum lipids were detected with automatic biochemistry analyzer and serum adiponectin,hs-CRP, TNF-α were measured using enzyme-linked immunosorbent assy(ELISA). Immunohistochemistry was used for analysis the expression levels of ICAM-1、VCAM-1and NF-κ B on the aortic wall.Results:1.Compared with AS model group, the levels of total cholesterol(TC), triglycerides(TG),low-density lipoprotein cholesterol (LDL-C) were lower(P<0.01orP<0.05) in baicalin high dose group and baicalin low dose group.2.The serum levels o f hs-CRP、TNF-α were significantly increased(P<0.01) and the level of serum adiponectin was significantly decreased(P<0.01) in AS model group;.However, Compared with AS model group, the serum levels o f hs-CRP、 TNF-α were markedly decreased(P<0.01or P<0.05) and the level of serum adiponectin was significantly enhanced(P<0.05) in baicalin high dose group and baicalin low dose group.3.Oil red O staining:There is no abnormalities in normal control group,and aortic lumen wall is smooth; it can be see intimal thickening, the lipid streaks and fibrous plaques in model group,and observed orange-red lipid infiltration;however, compared with model group, the thickness of the intimal were significantly thinner and orange-red lipid infiltration significantly decreased in baicalin low dose group. Baicalin high dose group has no obvious intima thickening, only a very small lipid infiltration. 4é After baicalin treatment, the expression levels of ICAM-1、VCAM-1、NF-κ B were significantly decreased(P<0.01).Conclusions:1. Baicalin through adjusting the lipid, improve the high condensation state and anti-inflammatory to prevent the development of atherosclerosis.2.Adiponectin could elevate by bacalin. Bacalin improves AS not only by reducing levels of serum lipids,the expression of inflammation factors, but also enhancing adiponectin levels.