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目的探讨罗格列酮(RGZ)对被动吸烟大鼠肺细胞凋亡蛋白表达的调节作用及其机制。方法采用熏烟的方法复制大鼠慢性阻塞性肺疾病(COPD)的动物模型,琼脂糖凝胶电泳检测DNA Ladder,免疫组织化学检测ASPP2和p53的表达,MTT检测罗格列酮体外对A549增殖的影响。结果模型组和RGZ预防组大鼠体重低于对照组。三组肺组织DNA琼脂糖凝胶电泳未检测到明显的细胞凋亡特征性DNA Ladder。模型组大鼠肺组织HE染色显示COPD的一些特征性变化:肺泡间隔增宽,肺泡融合,血管充血,用罗格列酮后,上述变化减轻。ASPP2和p53的表达变化类似:对照组几乎没有表达,模型组轻度表达,RGZ组表达下调。MTT实验罗格列酮体外对A549增殖无影响。结论罗格列酮能下调被动吸烟诱导的大鼠肺ASPP2和p53的表达。
Objective To investigate the regulatory effect of rosiglitazone (RGZ) on the expression of pulmonary apoptosis protein in passive smoking rats and its mechanism. Methods The model of chronic obstructive pulmonary disease (COPD) was established in rats by fumigation. The DNA ladder was detected by agarose gel electrophoresis. The expressions of ASPP2 and p53 were detected by immunohistochemistry. The proliferation of A549 cells was detected by MTT assay Impact. Results The body weight of model group and RGZ prevention group was lower than that of control group. DNA ladder was not detected on DNA agarose gel electrophoresis in three groups of lung tissues. HE staining of lung tissue in the model group showed some characteristic changes of COPD: broadening of the alveolar space, alveolar fusion, blood vessel congestion, rosiglitazone, the above changes were alleviated. The changes of ASPP2 and p53 were similar: the control group had almost no expression, the model group was mildly expressed, and the RGZ group was down-regulated. MTT experiment Rosiglitazone had no effect on the proliferation of A549 in vitro. Conclusion Rosiglitazone can down-regulate the expression of ASPP2 and p53 in rat lung induced by passive smoking.