摘要
目的探讨新型棉酚衍生物ApoG2和紫杉醇(PTX)联用对鼻咽癌的体内外抑制作用及可能机制。方法将不同浓度PTX、ApoG2单药及两药联用作用于人鼻咽癌CNE-2细胞48 h,采用MTT法检测细胞增殖抑制率;流式细胞仪检测细胞凋亡率。将12只CNE-2鼻咽癌皮下移植瘤裸鼠模型随机分为四组,对照组不干预,ApoG2组、PTX组及联合组分别予ApoG2、PTX及ApoG2与PTX联合应用(腹腔给药)。观察移植瘤生长情况,计算抑瘤率;采用免疫组化SP法检测各组Bcl-2蛋白表达。结果 ApoG2与PTX单药对细胞的抑制作用随药物浓度提高而增强,呈浓度依赖性;联合用药有协同作用(CDI<1);联合组细胞凋亡率明显高于对照组及ApoG2组、PTX组,P均<0.01;与ApoG2组及PTX组比较,联合组肿瘤体积明显减小(P<0.01),抑瘤率明显升高(P<0.01);Bcl-2表达率显著减低,P均<0.01。结论 ApoG2与PTX联用可协同抑制鼻咽癌细胞及其移植瘤生长;其作用机制可能与下调Bcl-2蛋白表达有关。
Objective To study the inhibitation effect of gossypol derivvatives Apogossypolone （ApoG2） combined with paclitaxd（PTX） on nasopharyngeal careinoma cells in vitro and in vivo. Methods ApoG2, PTX or combination of ApoG2 and PTX was adopted on CNE-2 cells. The inhibitory rate was measured by method of MTT assay. The apotosis rate was determined by method of flow cytometry. Twelve nude mice bearing human nasopharyngealcarcinoma xenografted tumor were randomly divided into 4 groups, which was the control group, the ApoG2 group, the PTX group and the combination group. ApoG2 group, PTX group and combination group were administrated by intraperitoneal injection method with corre- sponding drugs. The inhibition rate of tumor growth and coefficient of drugs in interaction were calculated. The expression of Bcl-2 was detected by method of immunohistochemistry SP staining. Results MTT assay showed that CNE-2 cells were both inhibited by PTX or ApoG2 in a dose-dependent manner. Flow cytometry assay indicated that CNE-2 cells apotosis rate increased in combination group （ P 〈 0.01 ）. The apoptosis rate of combination group was higher than that of the other three groups（P 〈 0.01 ）. Compared with ApoG2 group and PTX group, the tumor volomes reduced and the inhibition rate in- cerased in combination group （P 〈0.01 ）. Immunohistochemistry showed that Bcl-2 protein of combination group was in- hibited significantly（P 〈 0.01 ）. Conclusion Nasopharyngeal careinoma ceils and xenografted tumor could be inhibited after the combination usage of ApoG2 and PTX, which may be associated with their down-regulation of Bcl-2.
出处
《山东医药》
CAS
2013年第6期21-24,共4页
Shandong Medical Journal
基金
广州市科技计划项目(2011y2-00019-3)
