七氟烷通过MAPK/STAT3信号通路诱导人口腔舌鳞状细胞癌Tca-8113细胞凋亡

目的:探究七氟烷对人舌鳞状细胞癌Tca-8113细胞的凋亡机制。方法:用2~10μmol/L七氟烷作用体外培养人舌鳞状细胞癌Tca-8113细胞。MTT实验检测细胞活力;Hochest/PI双染法以及流式细胞术检测细胞凋亡;Western blot法检测MAPK/STAT3信号通路中相关蛋白表达含量的变化以及通过加入MAPK抑制剂检测MAPK与STAT3信号通路的关系。结果:七氟烷对Tca-8113细胞具明显的杀伤效应,IC₅₀=8μmol/L。七氟烷能够诱导Tca-8113细胞凋亡,促进Bax、cle-cas-3、cle-PARP、p-p38及p-JNK蛋白的表达,抑制Bcl-2、p-STAT3蛋白的表达;加入MAPK抑制剂后,细胞中p-p38、p-JNK、cle-cas-3及cle-PARP表达量降低,p-STAT3、p-ERK表达量增多。结论:七氟烷可能通过调控MAPK/STAT3信号通路从而导致Tca-8113细胞发生凋亡。

Sevoflurane induces apoptosis via MAPK/STAT3 signaling pathway in human tongue squamous cell carcinoma Tca-8113 cells

Objective:To investigate the mechanism of sevoflurane(Sevo)on apoptosis of human squamous cell carcinoma Tca-8113 cells.Methods:Tca-8113 cells were in vitro cultured with Sevo of 2-10μmol/L.The effects of Sevo on the cells were examined by MTT assay,Hochest 33342/PI double staining and flow cytometry(FCM)for the detection of cell proliferation and apoptosis.Western blot was used to detect the expression of related proteins in MAPK/STAT3 signaling pathway,the relationship between MAPK and STAT3 signaling pathway was detected by pretreatment of the cells with MAPK inhibitor.Results:Sevo inhibited the prolifevation of Tca-8113 cells with IC₅₀ of 8μmol/L.Sevo induced apoptosis of Tca-8113 cells,increased the expression of Bax,cle-cas-3,cle-PARP,p-p38 and p-JNK;inhibited the expression of Bcl-2 and p-STAT3.After pretreatment MAPK inhibitor,the expression levels of p-p38,p-JNK,cle-cas-3 and cle-PARP were decreased,the expression levels of p-STAT3 and p-ERK were increased.Conclusion:Sevoflurane may induce apoptosis of Tca-8113 cells by regulating MAPK/STAT3 signaling pathway.