稳消Ⅱ方对实验兔动脉粥样硬化模型PPARγ信号通路的影响  

Effect of Wenxiao Ⅱ Decotion on PPARγ Signaling Pathway in Experimental Atherosclerotic Rabbits

作　　者：梁荣[1] 霍清萍[1] LIANG Rong;HUO Qingping(The Sixth People′s Hospital Affiliated to Shanghai Jiaotong University,Shanghai 200233,China)

机构地区：[1]上海交通大学附属第六人民医院,上海200233

出　　处：《中西医结合心脑血管病杂志》2019年第9期1321-1324,共4页Chinese Journal of Integrative Medicine on Cardio-Cerebrovascular Disease

基　　金：上海市中西医结合临床培育项目(No.ZY3-LCPT-2-2007);上海市第六人民医院预研基金项目(No.LYZY-0120)

摘　　要：目的观察稳消Ⅱ方对实验兔动脉粥样硬化模型过氧化物酶体增殖物激活受体γ(PPARγ)表达的影响,以进一步明确稳消Ⅱ方抗动脉粥样硬化的作用机制。方法将健康新西兰大白兔38只随机分为空白组(9只)与造模组(29只),予高脂饲料造模8周后建立兔动脉粥样硬化模型。随后将造模组随机分为模型组、稳消Ⅱ方组、对照组,分别予生理盐水、稳消Ⅱ方、辛伐他汀干预8周后,处死全部实验兔,免疫组化法测得各组腹主动脉内皮细胞PPARγ阳性表达面积。在实验过程中分别检测造模前、造模后、干预后总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白(HDL)、低密度脂蛋白(LDL)水平。结果干预后,稳消Ⅱ方组、对照组TC、TG、LDL较模型组明显下降,HDL较模型组明显升高,差异均有统计学意义(P<0.05);稳消Ⅱ方组TC、TG、HDL、LDL与对照组相比,差异无统计学意义(P>0.05);稳消Ⅱ方组、对照组干预前后血脂水平比较差异有统计学意义(P<0.01)。模型组PPARγ表达水平较空白组明显下降(P<0.01);稳消Ⅱ方组、对照组PPARγ蛋白表达较模型组显著增加(P<0.05);对照组PPARγ蛋白表达水平略高于稳消Ⅱ方组,差异无统计学意义(P>0.05)。结论稳消Ⅱ方可激活PPARγ信号通路,上调PPARγ蛋白表达水平,从而起到稳定斑块、抑制动脉硬化发展的作用。Objective To investigate the effect of WenxiaoⅡdecotion(WXD)on lipid metabolism and peroxisome proliferator-activated receptor(PPAR)γsignaling pathway in experimental atherosclerotic rabbits,and to explore its mechanism.Methods Thirty-eight healthy New Zealand white rabbits were randomly divided into blank group(n=9)and model group(n=29).A model of atherosclerosis was established for 8 weeks of high fat diet.The rats in model group were randomly divided into model group,WXD group,and simvastatin control group,which were administrated by the normal saline,WXD,simvastatin for 8 weeks,respectively.The expression of PPARγprotein was detected by immunohistochemistry in abdominal aorta.The levels of total cholesterol(TC),triglyceride(TG),high density lipoprotein(HDL),and low density lipoprotein(LDL)were measured before and after modeling and after intervention.Results After intervention,compared with the model control group,the levels of TC,TG,and LDL in the simvastatin group and WXD group were significantly decreased while the HDL level was increased(P<0.05).There was no significant difference in the levels of TC,TG,HDL,and LDL between the simvastatin group and WXD group.After intervention,the expression level of PPARγin the model group was significantly lower than that in blank group(P<0.01).The expression of PPARγin simvastatin group and WXD group were significantly higher than that in the model group(P<0.05).The expression of PPARγprotein in simvastatin group was slightly higher than that in the WXD group,while there was no difference between two groups(P>0.05).Conclusion WXD can activate the PPARγsignal pathway,and up-regulate the expression level of PPARγprotein,thereby stabilizing plaque and inhibiting the development of arteriosclerosis.

关 键 词：动脉粥样硬化 稳消Ⅱ方 过氧化物酶体增殖物激活受体Γ 辛伐他汀 血脂 

分 类 号：R543.5[医药卫生—心血管疾病] R285.5[医药卫生—内科学]