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目的:研究肠复方对人大肠癌增殖和凋亡的影响。方法:采用瘤块接种法建立人大肠癌裸鼠原位移植瘤模型,将造模成功的50只裸鼠随机分组至肠复方高、中、低剂量组,氟尿嘧啶(5-Fu)组和模型对照(NS)组,每组10只。给药4周后,取下瘤体。采用HE染色,在光镜下观察细胞凋亡形态,TUNEL法原位缺口末端标记检测细胞凋亡,免疫组化原位检测细胞增殖细胞核抗原PCNA表达状态。结果:与模型对照组比较,肠复方高、中、低剂量组与氟尿嘧啶组瘤体细胞均有不同程度凋亡,其中肠复方高剂量组、中剂量组,5-FU组与模型对照组差异有统计学意义(P<0.01),肠复方低剂量组与模型对照组差异有统计学意义(P<0.05)。与模型对照组相比,肠复方中剂量组、5-FU组PCNA的表达均有所降低,与模型对照组差异有统计学意义(P<0.05)。肠复方高剂量组明显抑制细胞PCNA的表达,与模型对照组比较差异有统计学意义(P<0.01)。结论:肠复方能够诱导肠癌原位移植裸鼠移植瘤细胞凋亡,抑制细胞增殖,可能为肠复方抑瘤作用的机制之一。
Objective: To study the effect of Changfu Recipe on the proliferation and apoptosis of human colorectal cancer. Methods: Tumor nude inoculation method was used to establish orthotopic xenograft model of human colorectal cancer in nude mice. Fifty successful nude mice were randomly divided into five groups: high, medium and low dose group, 5-FU group and model Control (NS) group, 10 rats in each group. After 4 weeks of administration, the tumor was removed. The morphology of apoptotic cells was observed under light microscope by HE staining. Apoptosis was detected by TUNEL in situ nick end labeling. The expression of proliferating cell nuclear antigen PCNA was detected by immunohistochemistry in situ. Results: Compared with the model control group, the tumor cells of enteric compound high, medium and low dose groups and 5-fluorouracil group all had different degree of apoptosis, among which the high dose group, middle dose group, 5-FU group and model control group (P <0.01). There was a significant difference between the low-dose group and the model control group (P <0.05). Compared with the model control group, the expression of PCNA in the middle-dose group and the 5-FU group was significantly lower than that in the model control group (P <0.05). Intestinal compound high-dose group significantly inhibited the expression of PCNA, compared with the model control group, the difference was statistically significant (P <0.01). Conclusion: Changfu decoction can induce the apoptosis of xenografted human colon cancer xenografts in nude mice and inhibit cell proliferation, which may be one of the mechanisms of inhibiting the growth of intestine.