摘要
目的:探讨金黄色葡萄球菌杀白细胞素S组分(LukS-PV)通过活化补体5受体(C5aR)对非小细胞肺癌(NSCLC)细胞A549和H460凋亡的影响。方法:将敲低C5aR表达的慢病毒载体转染至A549和H460细胞中,qRT-PCR和Western blot检测C5aR敲低率,Annexin V/PI染色法检测敲低C5aR对细胞凋亡的影响。对敲低C5aR的细胞再加入LukS-PV,通过Annexin V/PI染色法和凋亡相关蛋白检测细胞凋亡情况。结果:与PBS对照组相比,LukS-PV可促进A549和H460细胞凋亡(P<0.05)。慢病毒载体转染A549和H460细胞敲低C5aR后,细胞C5aR表达水平降低(P<0.05)。在敲低C5aR基础上再加入LukS-PV,细胞凋亡受到抑制(P<0.05)。结论:敲低C5aR可抑制LukS-PV诱导NSCLC细胞的凋亡。
Objective:To investigate the effect of staphylococcal bicomponent LukS-PV leukocidin on the apoptosis of non-small cell lung cancer(NSCLC)cell lines A549 and H460 mediated by the C5a receptor(C5aR).Methods:Lentiviral vector with knockdown C5aR was transfected into A549 and H460 cells.qRT-PCR and Western blot were performed to measure the knockdown rate of C5aR.Annexin V/PI staining was used to determine the effect of C5aR knockdown on the cell apoptosis.Cells with C5aR knockdown were treated with LukS-PV.Annexin V/PI staining and apoptosis related proteins were then used to detect the cell apoptosis.Results:Compared with PBS control group,LukS-PV significantly promoted the apoptosis of A549 and H460 cells(P<0.05).C5aR expression was markedly decreased after knockdown of C5aR in the A549 and H460 cells transfected with lentiviral vector(P<0.05),and the apoptosis was inhibited when the cells further treated with LukS-PV after knockdown of C5aR(P<0.05).Conclusion:Knockdown of C5aR can inhibit LukS-PV induced apoptosis in NSCLC cells.
作者
张鹏
王杨燕
李婕
ZHANG Peng;WANG Yangyan;LI Jie(Department of Laboratory Medicine,The First Affiliated Hospital of Wannan Medical College,Wuhu 241001,Anhui,China)
出处
《皖南医学院学报》
CAS
2024年第1期24-27,32,共5页
Journal of Wannan Medical College
基金
皖南医学院重点项目科研基金(WK2021ZF20)。
