中文摘要：

目的探讨衣霉素（tunicamycin，TM）联合奥沙利铂（oxaliplatin，L—OPH）对人口腔癌KB细胞增殖和凋亡的影响及其相关分子机制。方法MTF法检测药物对KB细胞增殖抑制的影响；集落克隆形成法检测药物对KB细胞增殖的影响；碘化丙啶（propidiumiodide，PI）单染流式细胞仪检测KB细胞凋亡；半胱氨酸天冬氨酸蛋白酶3（Caspase-3）活性检测试剂盒检测Caspase一3的活性变化；Westernblot检测：Caspase-3、半胱氨酸天冬氨酸蛋白酶12（Caspase-12）及葡萄糖调节蛋白78（glucoseregulatedprotein78，GRP78）的表达。结果不同浓度衣霉素和（或）奥沙利铂对人口腔癌KB细胞具有增殖抑制作用，0．125μmol．L-1。衣霉素处理人口腔癌KB细胞的24、48、72h后细胞的存活率分别为90．37％、89．44％、88．91％。0．125μmol·L-1衣霉素与1μmol·L-1奥沙利铂联合使用对人口腔癌KB细胞24、48、72h的存活率低于单用衣霉素、奥沙利铂组，分别为50．78％、37．77％、23．24％；0．25μmol·L-1衣霉素可增强奥沙利铂抑制人口腔癌细胞KB的集落克隆形成的作用。0．5μmol·L-1衣霉素诱导KB细胞48h的凋亡率为8．3％。0．5μmol·L-1衣霉素与1μmol·L-1奥沙利铂联合刺激人口腔癌细胞KB48h的凋亡率为50．3％，高于奥沙利铂本身诱导的凋亡率24．6％。衣霉素上调GRP-78的表达以及增强联合用药组Caspase-3的活性及表达。结论衣霉素具有增强L—OPH抑制人口腔癌细胞增殖的作用，并增强奥沙利铂诱导人口腔癌细胞的凋亡，其机制可能是通过引起过度的内质网应激反应以及增加Caspase-3的活性。

英文摘要：

influence; the cell apoptosis was analyzed using flow cytometry with propidium iodide staining. Caspase-3 active detection kit was employed for detection of the drug effect within 24 h on Caspase-3 activity change; Western blot was applied to test Caspase-3, Caspase- 12 protein expression and protein expression of glucose regulation 78. Results The different concentrations of tunicamycin and/or oxaliplatin had significant prolifer- ation inhibition on oral cancer KB cells （The cell survival rate of 0. 125 μmol·L-1 tunicamycin adminis- tered in oral cancer KB cells after 24,48,72 h was 90.37% ,89.44% and 88.91% respectively）, While that of 0. 125 μmol·L-1 tunicamycin combined with 1μmol·L-1 oxaliplatin applied in oral cancer KB cells after 24,48,72 h was lower than that of the single dose of tunicamycin or oxaliplatin. The survival rate of three groups was 50. 78%, 37.77%, 23.24%, respectively. 0.25 μmol·L-1 tunicamycin can enhance the action of oxaliplatin on oral cancer cells KB colony clone for- mation. The apoptotic rate of 0. 5μmol·L-1 tunicamy- cin induced KB cells after 48 h was 8.3 % , and that of 0. 5 μmol·L-1 tunicamycin and 1μmol·L-1 oxali- platin stimulating human oral cancer cells KB after 48 h was 50.3%, Which was higher than the apoptotic rate of 24.6% incuced only by oxaliplatin. Tunicamycin could raise GRP-78 expression and enhance Caspase-3 activity and expression in combined treat- ment group. Conclusion Tunicamycin can enhance the proliferation inhibition and apoptosis inducement caused by oxaliplatin in oral cancer cells, and the mechanism may be caused by excessive endoplasmic reticulum stress reaction and increase of Caspase-3 ac- tivity.