基于JAK-STAT通路研究槲皮素对人宫颈癌C-33A细胞的影响

Study on the Effect of Quercetin on Human Cervical Cancer C-33A Cells Based on JAK-STAT Pathway

目的:观察槲皮素对人宫颈癌C-33A细胞凋亡的影响及对细胞周期的阻滞作用,探讨其可能作用机制。方法:将C-33A细胞分为对照组及槲皮素不同浓度(20μmol·L^(-1)、40μmol·L^(-1)、80μmol·L^(-1))组。MTT法检测细胞增殖抑制率,流式细胞术检测细胞凋亡率和细胞周期变化,Western blot法检测蛋白酪氨酸激酶2(JAK2)、p-JAK2、信号传导及转录活化因子3(STAT3)、p-STAT3蛋白表达。结果:与20μmol·L^(-1)组比较,40μmol·L^(-1)组及80μmol·L^(-1)组抑制率升高,且随着时间延长抑制率升高(P<0.05);与对照组比较,槲皮素不同浓度组凋亡率、G1期细胞百分率升高,S期细胞百分率和G2/M期细胞百分率、p-JAK2/JAK2、p-STAT3/STAT3水平明显降低(P<0.05),且呈浓度依赖性。结论:槲皮素可抑制C-33A细胞增殖并诱导细胞凋亡,阻滞细胞周期,其机制可能与阻断JAK/STAT通路有关。

Objective:To observe the effect of quercetin on the apoptosis of human cervical cancer C-33 A cells and its blocking effect on the cell cycle,and explore its possible mechanism.Methods:C-33 A cells were divided into control group and groups with different concentrations of quercetin(20μmol·L^(-1),40μmol·L^(-1),80μmol·L^(-1)).MTT method was used to detect cell proliferation inhibition rate,flow cytometry was used to detect cell apoptosis rate and cell cycle changes,and Western blot method was used to detect protein tyrosine kinase 2(JAK2),p-JAK2,signal transduction and activator of transcription 3(STAT3),p-STAT3 protein expression.Results:Compared with the 20μmol·L^(-1) group,the inhibition rate of the 40μmol·L^(-1) group and the 80μmol·L^(-1) group increased,and the 80μmol·L^(-1) group was higher than that of the 40μmol·L^(-1) group.The prolongation inhibition rate increased(P<0.05);compared with the control group,the apoptotic rate and the percentage of cells in G1 phase increased in the different concentrations of quercetin,the percentage of cells in S phase,the percentage of cells in G2/M phase,and the levels of p-JAK2/JAK2,p-STAT3/STAT3 decreased(P<0.05),and is concentration-dependent.Conclusion:Quercetin can inhibit the proliferation of C-33 A cells,induce apoptosis,and block the cell cycle.The mechanism may be related to blocking the JAK/STAT pathway.