过表达circ_0001105对脂多糖诱导的肺上皮细胞损伤凋亡及对炎症因子水平的影响  

Effects of overexpression of circ_0001105 on lipopolysaccharide-induced injury and apoptosis of lung epithelial cells and on the levels of inflammatory factors

作　　者：高翔[1] 庞琼[1] 王莹 GAO Xiang;PANG Qiong;WANG Ying(Department of Medical Oncology,Hanzhong Central Hospital,Hanzhong Shaanxi 723000,China)

机构地区：[1]汉中市中心医院肿瘤内科,陕西汉中723000

出　　处：《临床和实验医学杂志》2022年第23期2476-2480,共5页Journal of Clinical and Experimental Medicine

基　　金：陕西省重点研发计划项目(编号:2017SF-074)。

摘　　要：目的探讨circ_0001105对脂多糖(LPS)诱导的肺上皮细胞凋亡及炎症因子的影响及分子机制。方法本实验将肺上皮细胞A549分为Con组(没有处理的A549细胞)、LPS组(10 mg/L LPS处理A549细胞)、LPS+pcDNA组(pcDNA转染后用10 mg/L LPS处理)、LPS+pcDNA-circ_0001105组(pcDNA-circ_0001105转染后用10 mg/L LPS处理)、LPS+anti-miR-NC组(anti-miR-NC转染后用10 mg/L LPS处理)、LPS+anti-miR-155组(anti-miR-155转染后用10 mg/L LPS处理)、LPS+miR-155组(miR-155转染后用10 mg/L LPS处理)、LPS+pcDNA-circ_0001105+miR-155组(pcDNA-circ_0001105+miR-155共转染后用10 mg/L LPS处理);用四甲基偶氮唑盐比色法和流式细胞术分别检测肺上皮细胞的活性和凋亡情况;酶联免疫吸附试验检测肿瘤坏死因子α(TNF-α)、白细胞介素(IL)6、IL-8水平;双荧光素酶报告实验检测circ_0001105和miR-155的靶向关系。结果LPS诱导的肺上皮细胞的活性降低,细胞凋亡率升高,C-caspase3和C-caspase9表达水平升高,TNF-α、IL-6、IL-8水平升高,差异均有统计学意义(P<0.05)。circ_0001105靶向miR-155。过表达circ_0001105或下调miR-155能够逆转LPS诱导细胞活性降低、细胞凋亡增加以及TNF-α、IL-6和IL-8的释放,差异均有统计学意义(P<0.05)。而circ_0001105可通过靶向调控miR-155可显著逆转circ_0001105对肺上皮细胞凋亡及炎症因子的以上变化,差异均有统计学意义(P<0.05)。结论过表达circ_0001105可通过靶向下调miR-155抑制LPS诱导的肺上皮细胞凋亡及炎症因子释放,因此未来有一定潜力成为急性肺损伤的治疗靶点。Objective To explore the effect of circ_0001105 on lipopolysaccharide(LPS)-induced lung epithelial cell apoptosis and inflammatory factors and its molecular mechanism.Methods In this experiment,lung epithelial cells A549 were transfected with pcDNA,pcDNA-circ_0001105,anti-miR-NC,anti-miR-155,or miR-155 and then treated with 10 mg/L LPS,generating LPS group,LPS+pcDNA group,LPS+pcDNA-circ_0001105 group,LPS+anti-miR-NC group,LPS+anti-miR-155 group,LPS+miR-155 group,and LPS+pcDNA-circ_0001105+miR-155 group,and untreated A549 cells were used as a control(Con group).The activity and apoptosis of lung epithelial cells was detected by tetramethylazolium salt colorimetry(MTT)and flow cytometry;the levels of tumor necrosis factor alpha(TNF-α),interleukin(IL)-6,and IL-8 were detected by enzyme-linked immunosorbent assay;the targeting relationship of circ_0001105 and miR-155 was detected by dual luciferase reporter assay.Results LPS-induced lung epithelial cell activity was decreased,apoptosis rate was increased,the production of C-caspase3 and C-caspase9 was increased,and the levels of TNF-α,IL-6,IL-8 were increased(P<0.05).Circ_0001105 targeted miR-155 in A549 cells.Overexpression of circ_0001105 or down-regulation of miR-155 attenuated LPS treatment-induced inhibition in cell activity and promotion in cell apoptosis and levels of TNF-α,IL-6,and IL-8(P<0.05).However,circ_0001105 could significantly reverse the above changes of circ_0001105 on lung epithelial cell apoptosis and inflammatory factors by targeting miR-155(P<0.05).Conclusion Overexpression of circ_0001105 can inhibit LPS-induced lung epithelial cell apoptosis and inflammatory factor release through targeted downregulation of miR-155,so it has the potential to become a therapeutic target for acute lung injury in the future.

关 键 词：circ_0001105 MIR-155 肺上皮细胞 凋亡 炎症因子 

分 类 号：R563[医药卫生—呼吸系统]