摘要
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 explore the effect and mechanism of rosiglitazone （RGZ） on rat lung cell apoptosis induced by passive smoking. Methods Rat model of COPD was duplicated with passive smoking. Agarose gel electrophoresis was used to detect DNA Lad- der. fmmunohistochemistry was used to detect the expression of ASPP2 and p53. MTY assay was used to detect the effect of rosiglitazone on proliferation of A549 in vitro. Results The weights of rats in model group and RGZ group were lower than that of control group （ P 〈 0.05）. Apoptotic DNA Ladder was not obvious in agarose gel electrophoresis in all groups. The results of HE staining of model rats showed some features of COPD ： the widening alveolar septa of the passive smoking group, alveolar fusion, and vascular congestion, which had been alleviated in RGZ group. The expression of ASPP2 and p53 showed similar change ： no or weak expression in control group, mild expression in model group, while the expression levels was down-regulated in RGZ group. Rosiglitazone had no effect on the proliferation of A549 in vitro by MTT ASSAY. Conclusion Rosiglitazone can down-regulate ASPP2 and p53 expression induced by passive smoking.
出处
《中国微生态学杂志》
CAS
CSCD
2013年第9期1018-1020,1024,共4页
Chinese Journal of Microecology
基金
大连医科大学大学生科技创新基金
大连市科委项目资助(2006E13SF152)
