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目的:观察沙利度胺对人肝癌(HCC)细胞株SMMC7721裸鼠移植瘤生长和对SMMC7721细胞的血管内皮生长因子(VEGF)蛋白表达以及凋亡的影响。方法:建立BALB/c裸鼠皮下HCC细胞株SMMC7721移植瘤模型后,随机分为3种浓度沙利度胺实验组、阴性及阳性对照组,分别于第1天、第10天、第20天开始每日腹腔给药,连续4周后处死裸鼠,观察肿瘤生长情况,称瘤重,计算抑瘤率,免疫组化方法检测肿瘤组织中VEGF表达,流式细胞仪测肿瘤细胞凋亡。结果:不同浓度、不同给药时间沙利度胺组间抑瘤率比较,差异无统计学意义,P>0.05;各实验组与对照组瘤重比较,阴性对照组>沙利度胺实验组>阳性对照组,差异有统计学意义,P<0.05。不同给药时间沙利度胺组间瘤细胞VEGF蛋白表达比较,给药时间越早,VEGF蛋白表达越低,差异有统计学意义,P<0.05;不同给药浓度沙利度胺组间比较,差异无统计学意义,P>0.05;各实验组与对照组比较,差异有统计学意义,P<0.05。不同给药时间沙利度胺组瘤细胞凋亡率比较,给药时间越早,凋亡率越高,差异有统计学意义,P<0.05;不同给药浓度沙利度胺组间比较,差异无统计学意义,P>0.05;实验组凋亡率与对照组比较,差异有统计学意义,P<0.05。结论:沙利度胺抗裸鼠HCC细胞株SMMC7721移植瘤生长与治疗开始时间密切相关,而与药物浓度无明显相关性。其发挥抗肿瘤作用的关键机制可能为下调VEGF表达、促肿瘤细胞凋亡。
Objective: To observe the effects of thalidomide on the growth of xenografted human hepatoma (HCC) SMMC7721 xenografts and the expression of vascular endothelial growth factor (VEGF) protein and the apoptosis of SMMC7721 cells. Methods: The subcutaneous HCC cell line SMMC7721 xenografts in BALB / c nude mice were established and randomly divided into 3 groups: thalidomide experimental group, negative control group and positive control group, respectively. On day 1, day 10, day 20 The mice were sacrificed 4 weeks after the operation. The growth of the tumor was observed and the tumor weight was calculated. The tumor inhibition rate was calculated. The expression of VEGF in tumor tissue was detected by immunohistochemistry and the apoptosis of tumor cells was detected by flow cytometry. Results: There was no significant difference in inhibition rates between thalidomide groups at different concentrations and different administration time (P> 0.05). The tumor weight in each experimental group and control group was significantly lower than that in the negative control group > Positive control group, the difference was statistically significant, P <0.05. The expression of VEGF protein in thalidomide group at different administration time was earlier than that in the control group, and the earlier the administration was, the lower the expression of VEGF protein was, the difference was statistically significant, P <0.05; , The difference was not statistically significant, P> 0.05; the experimental group and the control group, the difference was statistically significant, P <0.05. Compared with the thalidomide group, the apoptosis rate of thalidomide group at different administration time was earlier, the administration time was earlier and the apoptosis rate was higher, the difference was statistically significant, P <0.05; The difference was not statistically significant (P> 0.05). The apoptosis rate in the experimental group was significantly different from that in the control group (P <0.05). CONCLUSIONS: Thalidomide is closely related to the initiation of treatment in HCC cell line SMMC7721 xenografts in nude mice, but not with the concentration of thalidomide. The key mechanism of its anti-tumor effect may be to down-regulate the expression of VEGF and promote tumor cell apoptosis.