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探讨细胞凋亡及凋亡调控基因在大鼠烟雾吸入性损伤发生、发展中的作用及意义。以大鼠烟雾吸入伤为模型 ,应用TUNEL、免疫组化及RT PCR技术 ,观察烟雾吸入伤后不同时相肺组织中Bcl 2、Bax、Fas、Fas配体 (FasL)基因mRNA及蛋白的表达状态及其与细胞凋亡异常之间的关系。结果显示 ,烟雾吸入伤后细胞凋亡指数升高 ;烟雾吸入伤后可上调Bcl 2、Bax、Fas、FasL表达 ,mRNA表达在 12h达峰值 ,蛋白表达在 2 4h最高。在各时相点Bax、Fas、FasL基因表达与肺组织细胞凋亡有正相关关系。提示烟雾吸入伤后细胞凋亡增加 ,细胞存活同时受生存基因 (Bcl 2 )和死亡基因 (Bax、Fas、FasL)的双重调控 ,凋亡相关基因参与了烟雾吸入伤过程细胞凋亡的调控。
To investigate the role and significance of apoptosis and apoptosis regulatory genes in the occurrence and development of smoke inhalation injury in rats. The smoke inhalation injury in rats was used as a model. The mRNA and protein expressions of Bcl-2, Bax, Fas and Fas ligand (FasL) mRNA in lung tissue were detected by TUNEL, immunohistochemistry and RT-PCR at different time points after inhalation of smoke State and its relationship with abnormal apoptosis. The results showed that the apoptotic index increased after inhalation of smoke. The expressions of Bcl 2, Bax, Fas and FasL were up-regulated after smoke inhalation injury. The mRNA expression peaked at 12h and the protein expression reached the peak at 24 h. There was a positive correlation between Bax, Fas, FasL gene expression and apoptosis of lung tissue at each time point. These results suggest that apoptosis increases after inhalation of smoke inhalation, and cell survival is regulated by Bcl-2 gene and death gene (Bax, Fas and FasL) simultaneously. Apoptosis-related genes are involved in the regulation of apoptosis during smoke inhalation injury.