【摘 要】
：
目的 探讨二甲双胍抑制腹主动脉瘤(AAA)形成的作用机制.方法 对10只8～10周龄ApoE-/-雄性小鼠高脂饮食并皮下植入含有血管紧张素Ⅱ的微量泵构建动脉瘤模型,均分为AAA组和二甲双胍干预组,4周后取材评估腹主动脉扩张情况,油红O染色观察血管外周脂肪细胞累积情况;免疫荧光染色和Western blot分析血管外周脂肪细胞的脂滴形成和缺氧诱导脂滴相关蛋白(HILPDA)的表达,qPCR检测血管外周脂肪组织中炎症因子的表达.结果 与AAA组比较,二甲双胍抑制了血管外周脂肪细胞的累积并减少脂肪细胞脂滴的形成
【机 构】
：
河北省唐山市人民医院内分泌科 063001;华北理工大学公共卫生学院,河北唐山 063210;河北医科大学附属第四医院心外科,石家庄 050000
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目的 探讨二甲双胍抑制腹主动脉瘤(AAA)形成的作用机制.方法 对10只8～10周龄ApoE-/-雄性小鼠高脂饮食并皮下植入含有血管紧张素Ⅱ的微量泵构建动脉瘤模型,均分为AAA组和二甲双胍干预组,4周后取材评估腹主动脉扩张情况,油红O染色观察血管外周脂肪细胞累积情况;免疫荧光染色和Western blot分析血管外周脂肪细胞的脂滴形成和缺氧诱导脂滴相关蛋白(HILPDA)的表达,qPCR检测血管外周脂肪组织中炎症因子的表达.结果 与AAA组比较,二甲双胍抑制了血管外周脂肪细胞的累积并减少脂肪细胞脂滴的形成;Western blot和qPCR检测结果发现HILPDA及相关炎症因子[肿瘤坏死因子(TNF)-α、白细胞介素(IL)-1β、IL-6]表达均降低(P<0.05).结论 二甲双胍可能通过调节HILPDA的表达减少血管外周脂肪细胞的累积和血管炎症,并最终抑制AAA的形成.
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