LncRNA MEG3靶向miR-138-5p对肺炎链球菌诱导的人肺泡上皮细胞损伤的影响OA

Objective:To investigate effect of long non-coding RNA maternally expressed gene 3(LncRNA MEG3)on apopto-sis and inflammatory damage of human pulmonary alveolar epithelial cells(HPAEpiC)induced by Streptococcus pneumoniae(SP)by targeting miR-138-5p.Methods:A pneumonia cell model was established in vitro by inducing HPAEpiC with SP,LncRNA MEG3 and miR-138-5p expressions were detected by qRT-PCR.HPAEpiC were grouped into Control group,Model group,sh-NC group,sh-MEG3 group,sh-MEG3+inhibitor NC group,sh-MEG3+miR-138-5p inhibitor group,miR-NC group and miR-138-5p group.qRT-PCR was used to detect LncRNA MEG3 and miR-138-5p expressions of HPAEpiC in each group;CCK-8 kit was used to detect proliferation ability;flow cytometry was used to detect apoptosis;ELISA was used to detect inflammatory factor levels;Western blot was used to detect Bax and Bcl2 proteins expressions.Targeting relationship between LncRNA MEG3 and miR-138-5p was validated.Results:Compared with Control group,LncRNA MEG3 expression,Bax protein expression,apoptosis rate,IL-6,TNF-α levels in HPAEpiC were unusually increased in Model group,while miR-138-5p expression,Bcl-2 protein expression,cell viability and IL-10 level were unusually decreased(P<0.05).Compared with sh-NC group,LncRNA MEG3 expression,Bax protein expression,apopto-sis rate,IL-6,TNF-α levels in HPAEpiC were prominently decreased in sh-MEG3 group,while miR-138-5p expression,Bcl2 protein expression,cell viability and IL-10 level were prominently increased(P<0.05).Compared with sh-MEG3+inhibitor NC group,Bax protein expression,apoptosis rate,IL-6,TNF-α levels in HPAEpiC were unusually increased in sh-MEG3+miR-138-5p inhibitor group,while cell viability,Bcl2 protein expression and IL-10 level were unusually decreased(P<0.05).Compared with miR-NC group,Bcl2 protein expression and IL-10 level in HPAEpiC were prominently increased in miR-138-5p group,while Bax protein expression,TNF-α,IL-6 levels and apoptosis rate were prominently decreased(P<0.05).Further experiment verified targeting rela-tionship between LncRNA MEG3 and miR-138-5p.Conclusion:LncRNA MEG3 is overexpressed in SP induced HPAEpiC.Knocking down LncRNA MEG3 inhibits HPAEpiC inflammatory response and apoptosis by up-regulating miR-138-5p.