lncRNA SNHG14调控肺炎链球菌感染的肺泡上皮细胞损伤的机制研究  

Mechanism of lncRNA SNHG14 modulating alveolar epithelial cells damage infected with Streptococcus pneumoniae

作　　者：谭清亚 牟方红 卿瑞 TAN Qingya;MOU Fanghong;QING Rui(Department of Respiratory and Critical Care Medicine,Kaizhou District People′s Hospital,Chongqing 405400,China)

机构地区：[1]重庆市开州区人民医院呼吸与危重症医学科,重庆405400

出　　处：《国际检验医学杂志》2025年第1期91-95,共5页International Journal of Laboratory Medicine

摘　　要：目的探讨长链非编码RNA SNHG14(lncRNA SNHG14)靶向miR-17-5p/叉头蛋白K2(FOXK2)轴对肺炎链球菌感染的肺泡上皮细胞增殖、凋亡和炎症反应的影响。方法将肺泡上皮细胞A549分为对照组、感染组、sh-NC组、sh-SNHG14组、sh-SNHG14+inhibitor NC组、sh-SNHG14+miR-17-5p inhibitor组。采用荧光定量PCR(RT-qPCR)法检测细胞lncRNA SNHG14、miR-17-5p、FOXK2 mRNA表达,CCK-8试剂盒检测A549细胞增殖,流式细胞术检测A549细胞的凋亡,酶联免疫吸附试验(ELISA)法检测细胞白细胞介素(IL)-1β、肿瘤坏死因子α(TNF-α)、IL-6水平;采用双荧光素酶报告基因实验检测lncRNA SNHG14与miR-17-5p、miR-17-5p、FOXK2的结合情况。结果与对照组相比,感染组lncRNA SNHG14、FOXK2 mRNA表达水平、细胞凋亡率、IL-6、TNF-α、IL-1β水平均升高,miR-17-5p表达水平、吸光度(A)值均降低,差异有统计学意义(P<0.05);sh-SNHG14组lncRNA SNHG14、FOXK2 mRNA表达水平、细胞凋亡率、IL-6、TNF-α、IL-1β水平较感染组、sh-NC组均降低,miR-17-5p表达水平、A值较感染组、sh-NC组均升高,差异有统计学意义(P<0.05);sh-SNHG14+miR-17-5p inhibitor组FOXK2 mRNA表达水平、细胞凋亡率、IL-6、TNF-α、IL-1β水平较sh-SNHG14+inhibitor NC组均升高,miR-17-5p表达水平、A值较sh-SNHG14+inhibitor NC组均降低,差异有统计学意义(P<0.05)。双荧光素酶报告基因实验验证结果显示,lncRNA SNHG14与miR-17-5p、miR-17-5p与FOXK2均存在靶向关系。结论干扰lncRNA SNHG14表达可上调miR-17-5p的表达,下调FOXK2的表达,从而使肺炎链球菌感染的肺泡上皮细胞的凋亡及炎症反应受到抑制,并促进其增殖。Objective To investigate the impacts of long non-coding RNA SNHG14(lncRNA SNHG14)on proliferation,apoptosis,and inflammatory response of alveolar epithelial cells infected with Streptococcus pneumoniae by targeting the miR-17-5p/forkhead box K2(FOXK2)axis.Methods Alveolar epithelial cells A549 were divided into control group,infection group,sh-NC group,sh-SNHG14 group,sh-SNHG14+inhibitor NC group,and sh-SNHG14+miR-17-5p inhibitor group.The mRNA expressions of lncRNA SNHG14,miR-17-5p and FOXK2 were detected by RT-qPCR,the proliferation of A549 cells was detected by CCK-8 kit,and the apoptosis of A549 cells was detected by flow cytometry.The levels of IL-1β,TNF-αand IL-6 were detected by ELISA.Dual luciferase reporter gene assay was used to detect the binding of lncRNA SNHG14 to miR-17-5p,miR-17-5p and FOXK2.Results Compared with control group,lncRNA SNHG14,FOXK2 mRNA expression,cell apoptosis rate,IL-6,TNF-αand IL-1βlevels were increased in infection group,while miR-17-5p level and absorbance(A)value were decreased,with statistical significance(P<0.05).LncRNA SNHG14 and FOXK2 mRNA expression,cell apoptosis rate,IL-6,TNF-αand IL-1βlevels in sh-SNHG14 group were lower than those in infection group and sh-NC group,while miR-17-5p expression level and A value were higher than those in infection group and sh-NC group,and the differences were statistically significant(P<0.05).FOXK2 mRNA expression,apoptosis rate,IL-6,TNF-αand IL-1βlevels of sh-SNHG14+miR-17-5p inhibitor group were all increased compared with sh-SNHG14+miR-17-5p inhibitor group,and the miR-17-5p expression and A value were decreased compared with sh-SNHG14+inhibitor NC group,the differences were statistically significant(P<0.05).Dual luciferase reporter gene test results showed that lncRNA SNHG14 and miR-17-5p,as well as miR-17-5p and FOXK2 had a targeting relationship.Conclusion Interfering the expression of lncRNA SNHG14 can up-regulate the expression of miR-17-5p and down-regulate the expression of FOXK2,thus inhibiting the apoptosis and infla

关 键 词：小核仁RNA宿主基因14 微小RNA-17-5p/叉头蛋白K2轴 肺炎链球菌 肺泡上皮细胞 

分 类 号：R563.1[医药卫生—呼吸系统]