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目的:探讨大黄素增强吉西他滨对裸鼠SW1990细胞移植瘤的抑瘤作用及其机制。方法:在裸鼠SW1990细胞移植瘤的动物模型上,分为生理盐水组(N组),大黄素组(E组,40 mg.kg-1),吉西他滨组(G组,125 mg.kg-1),联合用药组(E+G组,大黄素40 mg.kg-1+吉西他滨80 mg.kg-1)。各组均采取腹腔注射药物,3 d 1次,前后共11次。观察各组用药过程中肿瘤体积、瘤重、体重的变化。末次用药后1周处死裸鼠取肿瘤组织。采用Tunel法检测各组肿瘤组织凋亡情况。采用免疫组织化学染色法和Western blot法检测肿瘤组织凋亡相关蛋白Bax,Bcl-2和Cytochrome C的表达变化。结果:末次用药后1周E+G组肿瘤体积和瘤重明显小于其他各组;Tunel法显示E+G组肿瘤细胞凋亡比其余各组显著增多;免疫组织化学染色和Western blot法显示E+G组的Bax,Cytochrome C的表达比其他各组显著增多,而Bcl-2的表达比其余各组明显降低,经计算Bcl-2/Bax显著下降。结论:大黄素能显著增强吉西他滨对裸鼠体内人胰腺癌SW1990细胞移植瘤的抑瘤效果,其机制可能是大黄素通过促进胰腺癌SW1990细胞中Bax的表达和抑制Bcl-2的表达,降低Bcl-2/Bax,继而促进线粒体Cytochrome C释放,从而增强吉西他滨对胰腺癌SW1990细胞移植瘤的促凋亡作用,达到增强吉西他滨在体内的抑瘤效果。
Objective: To investigate the effect of emodin on the anti-tumor effect of gemcitabine on the transplanted tumor of SW1990 in nude mice and its mechanism. Methods: The animal model of xenografted SW1990 cells was divided into four groups: normal saline group (N group), emodin group (E group, 40 mg.kg-1), gemcitabine group (G group, 125 mg.kg- 1), combination group (E + G group, emodin 40 mg.kg-1 + gemcitabine 80 mg.kg-1). Each group were given intraperitoneal injection of drugs, 3 d 1 times, before and after a total of 11 times. The changes of tumor volume, tumor weight and body weight in each group were observed. One week after the last administration, the mice were sacrificed and the tumor tissues were taken. Tunel method was used to detect the apoptosis of tumor tissue in each group. Immunohistochemical staining and Western blot were used to detect the expression of Bax, Bcl-2 and Cytochrome C in tumor tissues. Results: At 1 week after the last administration, the tumor volume and tumor weight of E + G group were significantly smaller than those of other groups. The Tunel method showed that the apoptosis of tumor cells in E + G group was significantly increased compared with the other groups. Immunohistochemical staining and Western blot showed that E + G group Bax, Cytochrome C expression significantly increased compared with other groups, and Bcl-2 expression was significantly lower than the other groups, Bcl-2 / Bax was significantly decreased. Conclusion: Emodin can significantly enhance the anti-tumor effect of gemcitabine on the transplanted human pancreatic cancer SW1990 cells in vivo in vivo. The possible mechanism is that emodin can inhibit Bcl-2 expression in pancreatic cancer cell line SW1990 and decrease Bcl- -2 / Bax, and then promote the release of mitochondrial Cytochrome C, thereby enhancing the pro-apoptotic effect of gemcitabine on pancreatic cancer SW1990 cell xenografts and enhancing the anti-tumor effect of gemcitabine in vivo.