胡桃醌通过p38/JNK MAPK信号通路调控口腔鳞癌Tac8113细胞增殖和凋亡

目的:探讨胡桃醌通过p38/c-Jun氨基末端激酶(JNK)丝裂原活化蛋白激酶(MAPK)信号通路调控口腔鳞癌Tac8113细胞增殖和凋亡。方法:体外培养口腔鳞癌Tac8113细胞,分别给予终浓度为0,5,10,20μmol·L^-1的胡桃醌,继续培养24 h,检测细胞增殖、细胞凋亡和活性氧(ROS)水平,同时检测Tac8113细胞中p38、p-p38、JNK、p-JNK和Caspase-3蛋白表达水平。结果:与空白对照组比较,给予胡桃醌处理后,Tac8113细胞增殖率降低,Tac8113细胞凋亡率和ROS水平增加(P<0.05),且随着胡桃醌剂量增加,细胞增殖率、凋亡率和ROS变化越显著(P<0.05)。与空白对照组比较,给予胡桃醌处理后,Tac8113细胞p38和JNK蛋白表达变化不显著(P>0.05);p-p38、p-JNK和Caspase-3蛋白表达增加(P<0.05),且随着胡桃醌剂量增加,增加越显著(P<0.05)。结论:胡桃醌可能通过激活p38/JNK MAPK信号通路来诱导Tac8113细胞凋亡,从而达到抑制Tac8113细胞的目的。

Regulation of Juglone on the Proliferation and Apoptosis of Oral Squamous Cell Carcinoma Tac8113 Cells through p38/JNK MAPK Signaling Pathway

Objective:To investigate the regulation of Juglone on the proliferation and apoptosis of oral squamous cell carcinoma Tac8113 cells through p38/JNK MAPK signaling pathway.Methods:Oral squamous cell carcinoma Tac8113 cells were cultured in vitro.The final concentration of walnut quinone was 0,5,10 and 20μmol·L^-1 for 24 hours.The cell proliferation,apoptosis and ROS were detected.The expression levels of p38,p-p38,JNK,p-JNK and Caspase-3 protein in Tac8113 cells were also detected.Results:Compared with those in the blank control group,the proliferation rate of Tac8113 cells intervened by Juglone was decreased,the apoptosis rate and ROS level of Tac8113 cells intervened by Juglone were increased(P<0.05),and the effect was in a concentration-dependent manner(P<0.05).Compared with those in the blank control group,the expressions of p38 and JNK protein in Tac8113 cells intervened by Juglone was not significantly changed after the treatment with juniper(P>0.05),and the expressions of p-p38,p-JNK and Caspase-3 protein in Tac8113 cells intervened by Juglone were increased(P<0.05).The p-p38,p-JNK and Caspase-3 protein were increased with the dose of Juglone(P<0.05).Conclusion:Juglone can induce the apoptosis of Tac8113 cells by activating p38/JNK MAPK signaling pathway resulting in inhibiting Tac8113 cells.