肿瘤坏死因子相关受体2介导的IRE1-JNK信号通路在染矽尘大鼠肺泡巨噬细胞凋亡中的作用

郭肖非; 王伟; 肖倩

doi:10.13213/j.cnki.jeom.2015.14404

肿瘤坏死因子相关受体2介导的IRE1-JNK信号通路在染矽尘大鼠肺泡巨噬细胞凋亡中的作用

Role of Necrosis Factor Receptor-Associated Factor 2 Induced IRE1-JNK Signaling Pathway inNanometer Silica Rat Treated Alveolar Macrophage Apoptosis

摘要

摘要:
目的通过抑制肿瘤坏死因子相关受体2(TNFR2)后观察纳米二氧化硅粉尘对肺泡巨噬细胞的损伤程度,并进一步探索由TNFR2参与的肌醇酶1(IRE1)-C-Jun氨基端激酶(JNK)信号通路在介导肺泡巨噬细胞凋亡中的作用。

方法将NR8383.1型大鼠肺泡巨噬细胞分为空白对照组、二氧化硅组(50 mg/mL)和抗TNFR2组(在二氧化硅组基础上添加10 μg/mL anti-TNFR2抗体),同时每组设立3个平行样,培养24 h后,检测各组肺泡巨噬细胞凋亡水平,IRE1-JNK信号通路相关蛋白(TNFR2、凋亡信号调控激酶1、JNK、激活蛋白1、Caspase12)含量。

结果空白对照组肺泡巨噬细胞凋亡水平,TNFR2、凋亡信号调控激酶1、JNK、激活蛋白1及Caspase12含量均低于二氧化硅组,抗TNFR2处理后上述指标均较二氧化硅组降低,但仍较空白对照组高。

结论 TNFR2可能在JNK-IRE1信号通路介导的肺泡巨噬细胞凋亡中发挥着重要作用。

Abstract:
Objective To assess the damage to alveolar macrophages (AM) treated by nanometer silica and blocked tumor necrosis factor receptor-associated factor 2(TNFR2),and to explore the role of TNFR2 in inositol requiring enzyme 1(IRE1)-c-Jun N-terminal kinase (JNK) signaling pathway induced AM apoptosis.

Methods AM were divided into blank control group,silica group (50 mg/mL),and anti-TNFR2 group (10 μg/mL anti-TNFR2 antibody was added to the silica group).After cultured for 24 h,AM apoptosis rate and the contents of TNFR2,apoptosis signal-regulating kinase 1 (ASK1),JNK,transcription factor activator protein 1(AP1),Caspase12 were detected.

Results Compared with the blank control group,the silica group showed higher levels of AM apoptosis rate,TNFR2,ASK1,JNK,AP1,and Caspase12.The levels of above indicators were lowered after anti-TNFR2 treatment compared with those of the silica group,but still higher than those of the blank control group.

Conclusion TNFR2 may play apotential important role in JNK-IRE1 signaling pathway induced AM apoptosisgroup

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