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[目的]以新的切入点探讨石棉引起肺泡上皮细胞凋亡的分子机制.[方法]石棉暴露下,应用免疫荧光染色免疫法和免疫印迹法观察Mitofusin 2(MFN2)的变化;分别用衣霉素(TN)、钙离子阻滞剂和MFN2RNAi处理A549细胞,观察内质网与线粒体空间距离的变化.[结果]石棉可使MFN2表达上调;与正常对照组比较,TN组、钙离子阻滞组和MFN2RNAi组内质网与线粒体间的间隙均明显缩短.[结论]MFN2在石棉肺的发生发展过程中起一定的作用.
[Objective] To explore the molecular mechanism of asbestosis-induced alveolar epithelial cell apoptosis with new entry point. [Methods] The changes of Mitofusin 2 (MFN2) were observed by immunofluorescence staining and immunoblotting under the exposure of asbestos. (TN), calcium blockers and MFN2RNAi were used to treat A549 cells. The spatial distance between endoplasmic reticulum and mitochondria was observed. [Results] Asbestos could up-regulate the expression of MFN2. Compared with normal control group, The gap between endoplasmic reticulum and mitochondria in MFN2RNAi group was significantly shortened. [Conclusion] MFN2 play a role in the development and progression of asbestosis.