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目的研究内质网应激(endoplasmic reticulum stress,ERS)标识物葡萄糖调节蛋白(glucose regulated protein,GRP)和CCAAT增强子结合蛋白同源蛋白(CCAAT/enhancerbinding protein homologous protein,CHOP)在人胚肺成纤维细胞凋亡过程中的表达变化,初步探讨毒胡萝卜素对人胚肺成纤维细胞凋亡的作用及部分机制。方法体外用毒胡萝卜素(TG)诱导人胚肺成纤维细胞(MRC-5)后,采用流式细胞仪检测细胞的凋亡变化,RT-PCR检测细胞中GRP78、CHOPmRNA的表达变化,Western blot检测GRP、CHOP及Caspase-3蛋白的表达情况。结果与对照组比较,经TG作用24 h后,细胞凋亡率增加,并呈浓度依赖性,差异具有统计学意义(P<0.05)。TG组在24 h的GRP、CHOP表达均高于对照组,差异具有统计学意义(P<0.05,P<0.01);同时不同刺激组中Caspase-3的表达高于对照组,差异具有统计学意义(P<0.01)。结论毒胡萝卜素可诱导人胚肺成纤维细胞发生凋亡,该凋亡可能与ERS有关。
Objective To investigate the effect of endogenous endoplasmic reticulum stress (ERS) markers glucose regulated protein (GRP) and CCAAT enhancer binding protein homologous protein (CHOP) Fibroblasts in the process of apoptosis changes in the preliminary study of thapsigargin on human embryonic lung fibroblasts apoptosis and part of the mechanism. Methods The apoptosis of human embryonic lung fibroblasts (MRC-5) induced by thapsigargin (TG) in vitro was detected by flow cytometry. The expression of GRP78 and CHOP mRNA was detected by RT-PCR. Western blot Detection of GRP, CHOP and Caspase-3 protein expression. Results Compared with the control group, the apoptotic rate increased in a concentration dependent manner after 24 h treatment with TG, the difference was statistically significant (P <0.05). The expression of GRP and CHOP in TG group was higher than that in control group at 24 h (P <0.05, P <0.01), and the expression of Caspase-3 in different stimulation group was higher than that in control group Significance (P <0.01). Conclusion thapsigargin can induce apoptosis in human embryo lung fibroblasts, which may be related to ERS.