激活TLR2通过促进神经细胞死亡诱导假激酶表达诱导肺上皮细胞凋亡

发布时间：2018-03-15 06:10

本文选题：Toll样受体　切入点：神经细胞死亡诱导假激酶　出处：《细胞与分子免疫学杂志》2014年08期 　论文类型：期刊论文

【摘要】：目的探讨特异性激活Toll样受体2(TLR2)对于小鼠MLE-12肺上皮细胞发生细胞凋亡的影响及其潜在的分子机制。方法应用(0、1、3.3、10、33)ng/mL的TLR2特异性配基PAM3CYS4处理24 h或用33 ng/mL PAM3CYS4处理0、8、16、24、36、48 h,激活肺上皮细胞MLE-12的TLR2,使用Western blot法检测神经细胞死亡诱导假激酶(NIPK)和活性caspase-3的蛋白表达,用TUNEL凋亡检测试剂盒检测细胞凋亡的情况。结果与正常培养的MLE-12细胞相比,特异性激活TLR2可以促进NIPK和活性caspase-3的表达增加,细胞凋亡的阳性细胞数目增加;使用siRNA技术特异性抑制NIPK的表达后,显著抑制活性caspase-3表达,凋亡细胞数减少。结论特异性激活TLR2可增加NIPK的表达,促进肺上皮细胞发生凋亡。
[Abstract]:Objective to investigate the effect of specific activation of Toll like receptor 2 (TLR2) on apoptosis of mouse MLE-12 pulmonary epithelial cells and its possible molecular mechanism. Methods the specific ligand PAM3CYS4 of TLR2 was treated with TLR2 specific ligand PAM3CYS4 of 3. 3ng- / mL for 24 h or with 33 ng/mL PAM3CYS4 for 24 648 h. TLR2 of active lung epithelial cells (MLE-12) was used to detect the protein expression of neuronal death induced pseudokinase (NIPK) and active caspase-3 by Western blot assay. Results compared with normal cultured MLE-12 cells, the specific activation of TLR2 could promote the expression of NIPK and active caspase-3, and increase the number of apoptotic positive cells. After the expression of NIPK was specifically inhibited by siRNA, the expression of active caspase-3 was significantly inhibited, and the number of apoptotic cells was decreased. Conclusion the specific activation of TLR2 can increase the expression of NIPK and promote the apoptosis of pulmonary epithelial cells.
【作者单位】：中国医学科学院北京协和医学院医药生物技术研究所;中国航天员科研训练中心;
【基金】：中国航天医学基础与应用国家重点实验室项目(SMFA12B07) 总装试验技术重大项目(2012SY54A001) 军队后勤科研项目(CWS11J176) 创新团队项目(KCRT111)
【分类号】：R329.2;Q255

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