摘要
目的探讨辣椒素对胰腺癌BXPC-3细胞裸鼠移植瘤的生长抑制作用及其机制。方法建立耐药胰腺癌BXPC-3细胞的裸鼠皮下移植瘤动物模型,将荷瘤鼠随机分为:对照组(control,N组)、吉西他滨组(GEM)、低剂量辣椒素组(L-CAP)和高剂量辣椒素组(H-CAP)。第3周开始分别给予溶媒(生理盐水)0.2毫升/只、吉西他滨100mg/kg、辣椒素10mg/kg和辣椒素20mg/kg治疗。3天1次,共8次。实验过程中称测量肿瘤体积,末次用药1周后处死裸鼠。免疫组织化学法检测肿瘤组织中Ki-67(细胞增殖因子)、XIAP(X连锁凋亡抑制蛋白)和NF-κB(核转录因子)的表达。采用RT-PCR检测核转录因子NF-κB和XIAP mRNA的表达。结果末次用药1周后H-CAP组肿瘤体积和质量明显小于其他各组。免疫组织化学染色结果显示L-CAP组和H-CAP组的NF-κB和XIAP蛋白的表达量明显低于N组和GEM组。H-CAP组Ki-67的表达量明显低于其他各组。RT-PCR结果显示L-CAP组和H-CAP组的NF-κB和XIAP mRNA的表达量明显低于N组和GEM组。结论辣椒素可以通过下调NF-κB和XIAP基因和蛋白表达,从而产生对胰腺癌BXPC-3细胞移植瘤的抑制作用。
Objective To investigate the antitumor effect of Capsaicin on pancreatic cancer BXPC -3 cell xenograft on athymic. Methods The models of BXPC - 3 cell xenograft on athymic mouse were established and randomized into four groups with intraperitoneal （IP） injection of different drugs ： group N （0.9% sodium chloride）, group GEM （ gemcitabine, 100mg/kg）, group L - CAP （ capsaicin 10mg/kg） and group H -CAP （capsaicin 20mg/kg in combination）. The drugs were injected once every 3 days,with 8 times in all. The mice were sacrificed 1 week after the last injection. The tumor volume, tumor weight and body weight were measured during the drug ther- apy. Immunohistochemistry （IHC） was performed to detect the expression of NF - κB, XIAP and Ki -67. RT - PCR was performed to detect the expression of NF - κB and XIAP mRNA. Results One week after the last administration, the mean tumor volume and tumor weight in group H - CAP were significantly decreased compared to the other groups （P 〈 0.05 ）. IHC analysis showed that the expression of NF - κB and XIAP were down regulated in L - CAP and H - CAP groups compared to the other two groups （ P 〈 0.05 ）. The expression of Ki - 67 was also down regulated significantly in H - CAP group compared to the other groups （P 〈 0.05 ）. RT - PCR analysis showed that the expression of NF - κB and XIAP mRNA in L - CAP and H - CAP groups were down regulated significantly compared to the other groups （P 〈 0.05）. Conclusion Capsaicin can inhibit the the growth of pancreatic cancer cell xenograft. Downregulation of NF - κB and XIAP is possibly one of the mechanisms.
出处
《医学研究杂志》
2012年第12期169-172,共4页
Journal of Medical Research
