关键词: 微小 RNA-101-3p, 肿瘤坏死因子受体相关因子6, 肺炎链球菌, 肺泡上皮细胞, 细胞凋亡, 炎症

Abstract: Objective To investigate the effect of microRNA-101-3p (miR-101-3p) on alveolar epithelial cell apoptosis induced by Streptococcus pneumoniae (SP) through targeting tumor necrosis factor receptor related factor 6 (TRAF6). Methods A549 cells were cultured. Dual-luciferase reporter assay was used to detect the binding of miR-101-3p with TRAF6. Real-time quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to detect the mRNA expression levels of miR-101-3p and TRAF6. Western blotting was used to detect the protein expression levels of TRAF6, activated caspase-3 (C-caspase-3) and C-caspase-9. Flow cytometry assay was used to detect cell apoptosis rate. Enzyme-linked immunosorbent assay (ELISA) was used to measure the levels of interleukin-6 (IL-6) and IL-10 in the cell supernatant. Results TRAF6 was targeted and negatively regulated by miR-101-3p (P < 0. 05). After SP induction, the expression level of miR-101-3p was decreased and the expression level of TRAF6 was increased, the level of IL-6 was increased and the level of IL-10 was decreased, the apoptosis rate was increased, the expression levels of C-caspase-3 and C-caspase-9 was increased (P< 0. 05). Overexpression of miR-101-3p could attenuate the injury induced by SP in A549 cells. Overexpression of TRAF6 could partially reverse the protective effect of miR-101-3p on SP-induced apoptosis in A549 cells (P< 0. 05). Conclusion miR-101-3p negatively regulates TRAF6 to protect alveolar epithelial cells from SP-induced apoptosis and inflammatory damage. 

Key words: microRNA-101-3p, tumor necrosis factor receptor-associated factor 6, Streptococcus pneumoniae, alveolar epithelial cells, apoptosis, inflammation