目的：观察过氧化物酶体增殖物激活受体γ( PPAR-γ)对香烟诱导大鼠慢阻肺模型肺血管炎症的作用,初步探讨其可能机制。方法40只雄性Wistar大鼠随机分为4组,正常对照组、慢阻肺模型组、罗格列酮组( ROSI组)和罗格列酮+BADGE( RB组),测量血管内径及外膜炎症细胞总数,免疫组化分析肺血管上皮细胞PPAR-γ和Toll样受体-4(TLR4)蛋白表达。结果慢阻肺模型组可见肺血管炎性细胞浸润及肺血管壁的厚度,其血管上皮细胞中PPAR-γ表达明显下降,而TLR4的表达增多,差异有统计学意义(P<0．05)；与慢阻肺模型组比较,ROSI组在诱导PPAR-γ表达增多的基础上,其肺血管炎症浸润及肺血管壁增厚程度有所减轻,伴随着TLR4表达的减少,差异有统计学意义( P<0．05)。结论罗格列酮可能通过活化PPAR-γ,从而减轻慢阻肺模型大鼠肺血管炎症及血管重塑程度,其机制可能是通过抑制炎症通路-TLR4途径实现的。%Objective By observing the act of agonist of PPAR-γon cigarette induced rat copd model’s pulmonary vascu-lar inflammation,we preliminary discuss the probable mechanism. Methods We randomly divided 40 male Wistar rats into four groups,the control group,the model group,the ROSI group and the RB group. We measured the vascular inner diameter and the to-tal amount of the inflammatory cells in the outer membrane,carried out immunohistochemical analysis on the expression of PPAR-γand TLR4 of pulmonary vascular epithelial cells. Results The inflammatory cell infiltration in pulmonary vascular and the thick-ness of the pulmonary vascular wall can be detected in the model group,and the expression of PPAR-γdecreased apparently,but the expression of TLR4 increased. The difference is significant(P<0. 05). Compared with the model group,the expression of PPAR-γincreased in the ROSI group,the degree of the thickness and infiltration reduced and the expression of TLR4 decreased. The differ-ence is significant(P<0. 05). Conclusion By activating PPAR-γ,Rosiglitazone can reduce the extent of vasculitis and vascular remodeling. The mechanism may be inhibiting TLR4 inflammatory pathway.
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