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[目的]探讨白介素-17A(IL-17A)对 HepG2 细胞凋亡的影响及作用机制.[方法]培养正常肝细胞(L-02)及肝癌细胞(Huh7、HepG2 和PLC/PRF/5),荧光实时定量PCR(qRT-PCR)、Western blot测定其细胞 IL-17A表达.然后取 HepG2 细胞,予重组 IL-17A(rIL-17A)和(或)髓细胞白血病因子-1(Mcl-1)siRNA处理,流式细胞术分析细胞凋亡率;qRT-PCR、Western blot 检测 Mcl-1 表达.[结果]相对于 L-02 细胞, Huh7、HepG2 和PLC/PRF/5 细胞 IL-17A mRNA与蛋白水平明显增加,以 HepG2 细胞最高(P ＜0.01).rIL-17A使 HepG2 细胞凋亡减少(P ＜0.01),Mcl-1 表达上调(P ＜0.01).Mcl-1 siRNA预处理则逆转 rIL-17A对 HepG2 细胞凋亡的抑制作用(P ＜0.05).[结论]肝癌细胞IL-17A呈高表达,IL-17A通过上调Mcl-1表达发挥抗 HepG2 细胞凋亡作用.“,”[Objective]To explore the effects of interleukin-17A (IL-17A)on apoptosis of HepG2 cell and investigate the novel mechanism.[Methods]Quantitative real-time PCR (qRT-PCR)and Western blot were used to detect IL-17A expression in normal hepatocytes (L-02)and hepatic cancer cell lines (Huh7,HepG2 and PLC/PRF/5).Subsequently,HepG2 cells were selected and treated with recombinant IL-17A (rIL-17A) and/or myeloid cell leukemia-1 (Mcl-1)siRNA.Apoptotic rate was analyzed by flow cytometry.The expres-sion of Mcl-1 was measured by qRT-PCR and Western Blot.[Results]Compared to those in L-02 cells,the mRNA and protein levels of IL-17A were significantly increased in Huh7,HepG2 and PLC/PRF/5 cells,and HepG2 cells had the highest expression (P ＜0.01).Administration of rIL-17A reduced apoptotic rate and in-creased Mcl-1 expression in HepG2 cells (P ＜0.01).However,siRNA-mediated knockdown of Mcl-1 re-versed the inhibitory effect of rIL-17A on HepG2 cell apoptosis (P ＜0.05).[Conclusion]IL-17A is highly ex-pressed in hepatic cancer cells.IL-17A reduces HepG2 cell apoptosis by upregulating Mcl-1 expression.