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作 者:张培 张凌楠 杨勇[1] 马向瑞 ZHANG Pei;ZHANG Lingnan;YANG Yong;MA Xiangrui(Department of Oral and Maxillofacial Surgery, Binzhou Medical University Hospital, Binzhou 256603, China;Department of Orthodontics, Binzhou Medical University Hospital, Binzhou 256603, China)
机构地区:[1]滨州医学院附属医院口腔颌面外科,山东滨州256603 [2]滨州医学院附属医院口腔正畸科,山东滨州256603
出 处:《口腔医学研究》2021年第6期509-513,共5页Journal of Oral Science Research
基 金:山东省自然科学基金博士基金(编号:ZR2018BH026)。
摘 要:目的:探讨莪术醇对人舌鳞状细胞癌Tca-8113细胞凋亡的影响及其可能机制。方法:采用不同浓度莪术醇处理Tca-8113细胞,MTT法检测细胞增殖活性;流式细胞术检测细胞凋亡水平和细胞线粒体膜电位变化;Western blot检测细胞中凋亡相关蛋白Bax、Bcl-2、Cleaved-caspase-3和p38 MAPK信号通路相关蛋白p-p38MAPK、p38MAPK以及线粒体和细胞质中Cyt C等蛋白表达水平。采用p38 MAPK抑制剂SB203580联合莪术醇处理Tca-8113细胞,流式细胞术检测细胞凋亡水平和细胞线粒体膜电位变化;Western blot检测细胞中p38 MAPK信号通路相关蛋白p-p38MAPK、p38MAPK表达水平。结果:莪术醇可呈时间和剂量依赖性抑制Tca-8113细胞增殖,诱导细胞凋亡,降低线粒体膜电位,并下调Bcl-2和线粒体中Cyt C蛋白表达水平,上调Bax、Cleaved-caspase-3、p-p38MAPK及细胞质中Cyt C蛋白表达水平,而对p38 MAPK蛋白表达水平无影响。然而,SB203580干预可抑制莪术醇对Tca-8113细胞凋亡、线粒体膜电位改变、p38 MAPK信号通路激活的诱导作用。结论:莪术醇可促进Tca-8113细胞凋亡,其机制可能与激活p38 MAPK介导的线粒体凋亡途径有关。Objective:To investigate the effect of curcumol on apoptosis of human tongue squamous cell carcinoma Tca-8113 cells and its possible mechanism.Methods:Tca-8113 cells were treated with curcumol at different concentrations.The cell proliferation was detected by MTT assay,apoptosis rate and mitochondrial membrane potential change were evaluated by flow cytometry,and the expression levels of apoptosis-related proteins(Bax,Bcl-2,and Cleaved-caspase-3)and p38 MAPK signaling pathway related proteins(p-p38MAPK,p38MAPK,and Cyt C)in mitochondria and cytoplasm were detected by Western blot.Tca-8113 cells were treated with p38 MAPK inhibitor SB203580 combined with curcumol.The apoptosis rate and mitochondrial membrane potential change were detected by flow cytometry,and the expression levels of p38 MAPK signaling pathway related proteins(p-p38MAPK and p38MAPK)were detected by Western blot.Results:Curcumol inhibited the proliferation of Tca-8113 cells in a time and dose-dependent manner.Meanwhile,Curcumol significantly induced apoptosis,reduced mitochondrial membrane potential,and down-regulated the protein expression levels of Bcl-2 and Cyt C in mitochondria,and up-regulated the protein expression levels of Bax,Cleaved-caspase-3,p-p38 MAPK,and Cyt C in the cytoplasm.There was no significant change in the expression of P38 MAPK protein.However,SB203580 intervention inhibited the inducing effect of curcumol on Tca-8113 cell apoptosis,mitochondrial membrane potential change,and activation of p38 MAPK signaling pathway.Conclusion:Curcumol can promote the apoptosis of Tca-8113 cells,the mechanism may relate to the activation of p38 MAPK-mediated mitochondrial apoptotic pathway.
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