摘要
目的探讨在动脉粥样硬化模型(AS)发生发展过程中VE-钙黏蛋白表达变化的意义及黄芩苷抗AS作用的可能机制。方法建立小鼠ApoE-/-AS模型,20只雄性ApoE-/-小鼠随机分为AS模型组及黄芩苷治疗组,每组10只;雄性C57BL/6小鼠10只为正常对照组。建模成功后,黄芩苷治疗组小鼠给予黄芩苷50 mg/(kg·d)灌胃,AS模型组及正常对照组给予生理盐水灌胃,连续灌胃4周。12周后处死动物,检测血清炎症指标,以及主动脉核因子-κB(NF-κB)、VE-钙黏蛋白的表达水平。结果模型成功后,小鼠主动脉NF-κB、VE-钙黏蛋白阳性表达及炎症因子水平与正常对照组比较明显升高(P<0.01或P<0.05),黄芩苷处理后,治疗组的小鼠主动脉NF-κB、VE-钙黏蛋白表达及炎症因子水平显著降低(P<0.01或P<0.05),VE-钙黏蛋白表达与NF-κB阳性表达及炎症因子水平呈正相关(r=0.77)。结论黄芩苷对AS有保护作用,其机制可能是通过降低NF-κB的转录活性、下调炎症因子以及VE-钙黏蛋白的表达,从而减轻内皮细胞损伤实现的。
Objective To study the effect of VE-cadherin expressions in the development of atherosclerosis （AS） and the possible mechanism of Baicalin in anti-AS. Methods ApoE -/- mice model of atherosclerosis （AS） was estab- lished. 20 male ApoE-/- mice were randomly divided into the model group and the baicalin treatment group. Ten C57BL/6 mice were chosen in the normal control group. 50 mg/（ kg · d） baicalin was given to mice in treatment group, and physiological saline was given to the mice in AS model group and normal control group for 4 weeks. After 12 weeks, the mice were put to death and the expression level of the serum inflammation biomarkers, aortic NF-KB and VE-cadherin were detected. Results NF-KB of aortic artery cells in mice, VE-cadherin positive expression and inflam- matory factor levels were obviously increased compared with the normal group （ P 〈 0.01 or P 〈 0.05 ）. After the treat- ment of baicalin, aortic artery cells NF-KB in mice, VE-cadherin expression and inflammatory factors in the treatment group were significantly reduced （P 〈0.01 or P 〈0.05 ）, which showed that VE-cadherin expression, the NF-KB ex- pression and inflammatory factor levels were positively related. Conclusion Baicalin could have certain protective effect and the mechanism may be related to reduction the NF-KB transcription activity, lower inflammatory factors and VE-cadherin, thereby reducing the injury of endothelial cell.
出处
《山东大学学报（医学版）》
CAS
北大核心
2013年第9期26-30,共5页
Journal of Shandong University:Health Sciences
基金
山东省科技攻关计划项目(2007GGB01357)
