NF-κB RNAi decreases the Bax/Bcl-2 ratio and inhibits TNF-α-induced apoptosis in human alveolar epithelial cells

被引:86
作者
Li, Li [1 ]
Wu, Weijing [2 ]
Huang, Wenjie [1 ]
Hu, Gen [1 ]
Yuan, Weifeng [1 ]
Li, Weifeng [1 ]
机构
[1] Guangzhou Mil Command, Guangzhou Gen Hosp, Dept Resp Med, Guangzhou 510010, Guangdong, Peoples R China
[2] Fujian Med Univ, Affiliated Hosp 2, Dept Resp Med, Quanzhou 362000, Fujian, Peoples R China
基金
中国国家自然科学基金;
关键词
Acute lung injury; Alveolar epithelial cells; Bax; Bcl-2; Nuclear factor-kappa B; ACUTE LUNG INJURY; RESPIRATORY-DISTRESS-SYNDROME; NEUTROPHIL APOPTOSIS; INFLAMMATION; DISEASES; ACTIVATION; TARGET;
D O I
10.1007/s00011-013-0590-7
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Apoptosis of alveolar epithelial cells (AECs) plays a key role in acute lung injury (ALI). Understanding the underlying mechanism is conducive to the treatment of ALI. The goal of this study was to determine the possible involvement of nuclear factor-kappa B (NF-kappa B)/p65 and Bax/Bcl-2 in tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis in AECs. Type II AECs, A549, with or without NF-kappa B/p65 expression silenced by small interfering RNA (siRNA) were challenged with TNF-alpha. The levels of NF-kappa B/p65, Bcl-2 and Bax were detected by reverse transcription-polymerase chain reaction, Western blotting, and immunocytochemical staining. The apoptosis rate was measured by flow cytometry. TNF-alpha challenge significantly increased the transcription and translation of NF-kappa B/p65 and Bax genes, but significantly decreased the Bcl-2 gene level. siRNA silencing of NF-kappa B/p65 reversed the effect of TNF-alpha on NF-kappa B/p65, Bcl-2 and Bax, and significantly decreased the TNF-alpha-induced apoptosis rate of AECs, as compared to the non-silenced cells. This study indicates that NF-kappa B plays an important role in the process of TNF-alpha-induced apoptosis in AECs, via regulation of the expression of Bcl-2 and Bax.
引用
收藏
页码:387 / 397
页数:11
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