论文部分内容阅读
目的:探讨大黄素(Emodin,EMO)在体内对胰腺癌BXPC-3细胞移植瘤的体内抑制作用,并探讨其初步机制。方法:建立胰腺癌裸鼠移植瘤模型,分为对照组(NS)、大黄素组(EMO)和吉西他滨组(Gemcitabine,GEM)3组,各组通过腹腔注射作用2周后,检测实验前后裸鼠体质量变化及抑瘤率,免疫组化检测细胞增殖因子ki-67的表达,TUNEL法检测移植瘤组织的细胞凋亡。结果:EMO组(25.1±1.58)g、和GEM(25.6±1.47)g组的动物体质量与对照组(27.0±1.64)g相比,无显著性差异;EMO组和GEM组的抑瘤率分别为38.46%和44.23%,免疫组化检测ki-67结果显示,与对照组IOD(219.5±17.98)相比,EMO组IOD(146.6±11.57)和GEM组IOD(139.5±12.55)明显减小(P<0.01),EMO组和GEM组间比较差异无统计学意义。TUNEL检测结果显示,与对照组IOD值(23.6±6.02)相比,EMO组IOD值(65.7±4.97)和GEM组IOD值(67.4±5.59)明显增大(P<0.01);EMO组和GEM组间比较差异无统计学意义。结论:大黄素可抑制胰腺癌细胞株BXPC-3细胞在裸鼠体内的生长;此作用机制可能为抑制肿瘤细胞增殖及促进肿瘤细胞的凋亡。
Objective: To investigate the in vivo inhibition of Emodin (EMO) on pancreatic cancer BXPC-3 cell xenografts and to explore its primary mechanism. Methods: The model of pancreatic cancer xenografts in nude mice was established and divided into 3 groups: control group (NS), emodin group (EMO) and gemcitabine group (GEM). The mice were injected intraperitoneally for 2 weeks. The changes of tumor weight and tumor inhibition rate were observed. The expression of cell proliferation factor ki-67 was detected by immunohistochemistry. The apoptosis of tumor tissue was detected by TUNEL. RESULTS: There was no significant difference in body weight between the EMO group (25.1 ± 1.58) g and the GEM (25.6 ± 1.47) g group compared with the control group (27.0 ± 1.64) g; the inhibition rates of EMO group and GEM group (38.46%) and 44.23% (44.23%) respectively. The results of immunohistochemical detection of ki-67 showed that IOD (146.6 ± 11.57) in EMO group and IOD (139.5 ± 12.55) in GEM group were significantly decreased compared with IOD (219.5 ± 17.98) (P <0.01). There was no significant difference between EMO group and GEM group. The results of TUNEL showed that the IOD of EMO group (65.7 ± 4.97) and the IOD value of GEM group (67.4 ± 5.59) were significantly higher than those of control group (23.6 ± 6.02) (P <0.01) There was no significant difference between groups. Conclusion: Emodin can inhibit the growth of pancreatic cancer cell line BXPC-3 in nude mice. The mechanism may be to inhibit tumor cell proliferation and promote tumor cell apoptosis.