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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 investigate the significance of VE-cadherin expression in the development of atherosclerosis model (AS) and the possible mechanism of the anti-AS effect of baicalin. Methods ApoE - / - AS mouse model was established. Twenty male ApoE - / - mice were randomly divided into AS model group and baicalin treatment group, with 10 mice in each group. Ten male C57BL / 6 mice served as normal control group. After the model was established, the baicalin-treated mice were given gavage baicalein 50 mg / (kg · d) orally. The rats in the AS model group and the normal control group were given gavage with normal saline for 4 weeks. After 12 weeks, the animals were sacrificed to detect serum inflammatory markers and the expression of aortic nuclear factor-κB (NF-κB) and VE-cadherin. Results After the model was successfully established, the positive expression of NF-κB, VE-cadherin and the level of inflammatory cytokines in the aorta of mice were significantly higher than those in the normal control group (P <0.01 or P <0.05). After treatment with baicalin, The levels of NF-κB, VE-cadherin and inflammatory cytokines were significantly decreased in the aorta of mice (P <0.01 or P <0.05). The expression of VE-cadherin was positively correlated with the expression of NF-κB and the level of inflammatory cytokines = 0.77). CONCLUSION: Baicalin can protect AS cells by down-regulating the transcriptional activity of NF-κB, down-regulating the expression of inflammatory cytokines and VE-cadherin, thereby reducing endothelial cell injury.