瓜蒌薤白半夏汤对动脉粥样硬化小鼠炎症因子、ICAM-1、VCAM-1表达的影响

摘要

目的:观察瓜蒌薤白半夏汤(GXBD)对Apo-E-/-小鼠动脉粥样硬化模型(AS)C反应蛋白(CRP)、白介素-6(IL-6)、肿瘤坏死因子(TNF-α)、细胞间黏附分子-1(ICAM-1)和血管细胞黏附分子-1(VCAM-1)表达的影响,并探讨其可能的机制.方法:以高脂饲料饲喂雄性Apo-E-/-小鼠建立AS模型,将AS模型小鼠随机分为模型对照组(MS)、辛伐他汀组(XFTT)、GXBD高、低剂量组,选取C57BI/6J雄性小鼠作为正常对照组,每组10只,连续灌胃(ig)给药8周.末次给药24h后,检测血清总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL-C)、高密度脂蛋白(HDL-C)、及血清CRP、IL-6、TNF-α水平,HE染色观察主动脉组织病理学变化;Western-Blot法检测主动脉VCAM-1和ICAM-1蛋白表达水平.结果:模型组小鼠TC、TG、LDL-C、HDL-C、及血清CRP、IL-6、TNF-α显著高于正常对照组(P＜0.05),主动脉VCAM-1、ICAM-1蛋白表达显著高于正常对照组(P＜0.05),模型组小鼠主动脉出现明显粥样硬化斑块;GXBD各组和辛伐他汀组小鼠血脂及血清CRP、IL-6、TNF-α水平显著低于模型组(P＜0.05),主动脉组织VCAM-1、ICAM-1蛋白表达水平显著低于模型组(P＜0.05),且主动脉组织粥样硬化病变明显减轻.结论:GXBD对Apo-E-小鼠AS病变有较好的治疗作用,其机制与其调节血脂代谢、抑制炎症因子及主动脉组织VCAM-1、ICAM-1蛋白的表达相关.%Aim:To observe the influence of Gualou Xiebai Banxia Decoction on atherosclerosis inflammatory factors,the expression of ICAM-1 and VCAM-1,and to explore its possible mechanisms.Methods:established the AS model of Apo-E-/-male mice with high fat diet,AS model mice were randomly divided into the model group,simvastatin group,GXBD high dose and low dose group,choosed C57BL/6J male mice as the normal control group,10 mice for each group and last for 8 weeks.Testing the levels of TC,TG,LDL-C,HDL-C,and CRP,IL-6,TNF-α.Observing the changes of tissues structure with HE staining,as well as detecting the expression levels of VCAM-1 and ICAM-1 on the method of Western-Blot.Results:The mice model blood lipid levels,serum CRP、IL-6、TNF-α levels were significantly higher than those of the control group (P ＜ 0.05),and the aortic VCAM-1,ICAM-1 expression was significantly higher than those of the control group (P ＜ 0.05),namely aortic atherosclerosis lesions evident;Meanwhile,at GXBD group and XF'TF group,lipids and serum CRP,IL-6,TNF-α significantly lower than those of the model group (P ＜ 0.05),VCAM-1,ICAM-1 expression were significantly lower than those of the model group (P ＜ 0.05),the difference were statistical significantly,Aortic atherosclerotic lesions were reduced namely.Conclusion:GXBD has a better therapeutic effect on AS Apo-E-/-mice lesions.The mechanism may be related to the regulation of lipid metabolism,inhibiting inflammatory cytokines and aortic VCAM-1,ICAM-1 protein expression.