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[目的]观察舒林酸对凋亡调控基因的影响,探讨舒林酸防治肿瘤的分子机制。[方法]利用二甲基苯并蒽诱发的实验性胰腺癌小鼠模型,采用免疫组化染色的方法分别标记p53、Bcl-2和Bax阳性细胞,分阶段动态观察舒林酸对各种蛋白表达的影响。[结果]随观察时间延长,p53表达逐渐增高,在各个实验阶段,预防组、治疗组的p53阳性率与对照组差异均有统计学意义(P<0.01);随实验观察时间延长,Bax呈逐渐升高趋势,而Bcl-2和Bax分别在第三和第二阶段达到峰值后呈下降趋势。至实验结束时,预防组Bcl-2以及Bax均低于对照组(P<0.05),而治疗组与对照组仅Bax差异具有统计学意义(P<0.01)。[结论]舒林酸可能通过抑制突变型p53和Bcl-2的表达,诱导细胞凋亡,从而抑制胰腺癌形成和发展。
[Objective] To observe the effect of sulindac on apoptosis regulatory genes and to explore the molecular mechanism of sulindac on tumor prevention and treatment. [Method] With the experimental model of pancreatic cancer induced by dimethylbenzanthracene, the positive cells of p53, Bcl-2 and Bax were labeled by immunohistochemical staining, and the effect of sulindac on various proteins The impact of expression. [Results] The expression of p53 increased gradually with the prolongation of observation time. The positive rates of p53 in the prevention group and the treatment group were significantly different from those in the control group at each experimental stage (P <0.01). With the prolonged experimental observation, the expression of Bax Gradually increased. However, Bcl-2 and Bax tended to decline after the third and second phases respectively. At the end of the experiment, the levels of Bcl-2 and Bax in the prophylaxis group were lower than those in the control group (P <0.05), while only the Bax difference between the treatment group and the control group was statistically significant (P <0.01). [Conclusion] Sulindac can inhibit the formation and development of pancreatic cancer by inhibiting the expression of mutant p53 and Bcl-2 and inducing apoptosis.