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目的:本实验通过观察舒林酸对凋亡调控基因的影响,初步探讨舒林酸防治肿瘤作用可能存在的分子机制。方法:利用二甲肼诱发的实验性大肠癌小鼠模型,采用免疫组化染色的方法,分别标记p53、Bcl-2和Bax阳性细胞,分阶段地动态观察舒林酸对各种蛋白表达的影响。结果:预防组、治疗组的p53阳性率与模型组差别均有统计学意义(P均<0.01);随实验观察时间延长,p53和Bax呈逐渐升高趋势,而Bcl-2和Bcl-2/Bax分别在第3和第2阶段达到峰值后呈下降趋势。至实验结束时,预防组p53、Bcl-2以及Bcl-2/Bax比值均低于模型组(除p53外,P均<0.05),而治疗组与模型组仅Bax之间差别具有统计学意义(P<0.01)。结论:舒林酸通过抑制突变型p53和Bcl-2的表达,诱导细胞凋亡,从而抑制肿瘤形成和发展。
Objective: In this experiment, we observed the effect of sulindac on apoptosis regulatory genes, and probed into the possible molecular mechanism of sulindac on the prevention and treatment of tumor. Methods: The mouse model of experimental colorectal cancer induced by dimethylhydrazine was used. The positive cells of p53, Bcl-2 and Bax were labeled by immunohistochemistry, and the expression of various proteins influences. Results: The positive rates of p53 and Bcl-2 in the prevention group and the treatment group were significantly different from those in the model group (all P <0.01). The p53 and Bax levels gradually increased with the prolonged experimental observation, while the expressions of Bcl-2 and Bcl-2 / Bax after the peak in the third and second phase, respectively, after a downward trend. At the end of the experiment, the ratio of p53, Bcl-2 and Bcl-2 / Bax in the prevention group was lower than that in the model group (P <0.05, except for p53), but there was a statistically significant difference between the treatment group and the model group (P <0.01). Conclusion: Sulindac inhibits the formation and development of tumor by inhibiting the expression of mutant p53 and Bcl-2 and inducing cell apoptosis.