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目的 探讨亚硒酸钠对实验性胃癌形成的作用及对p53和p16表达的影响。 方法 用N 甲基 N′ 硝基 N′ 亚硝基胍(MNNG)(20mg kg)给大鼠灌胃,每天1次,连续10d,以诱导大鼠胃癌形成。观察到实验的第43d, 用HE染色病理诊断和AB PAS方法探讨了硒在MNNG诱导Wistar大鼠胃癌形成过程中的作用,用免疫组织化学SP 法研究了在此过程中p53和p16蛋白的表达及其变化,并对以上结果进行定性、定位、图像分析和统计学处理。 结果 饮水中加入2mg/L和4mg/L的亚硒酸钠加重胃黏膜的糜烂、出血,促进胃黏膜的肠上皮化生(P<0.05),在 MNNG诱癌过程中发生了浆膜下平滑肌瘤,亚硒酸钠可以增加平滑肌瘤的发生率。免疫组织化学结果显示,p53阳 性产物定位在胞核和胞质,主要在胞质;实验对照组、低硒组、高硒组的p53蛋白染色的平均光密度(MA)明显高于 正常对照组(P<0.05,P<0.01)。p16蛋白阳性产物表达在大鼠胃腺和胃上皮细胞核内;实验对照组、低硒组、高硒 组的MA值比正常对照组略有升高(P>0.05)。 结论 在MNNG所致胃癌的过程中,饮水中加入2mg/L,4mg/L 亚硒酸钠可以促进胃黏膜的糜烂、出血、肠上皮化生,提示亚硒酸钠并不能降低大鼠胃癌的发生率,其机制可能与 抑癌基因p53的突变与p16的异常表达有关。
Objective To investigate the effect of sodium selenite on the formation of experimental gastric carcinoma and its effect on the expression of p53 and p16. Methods Rats were intragastrically infused with N-methyl N ’nitro-N’ nitrosoguanidine (MNNG) once daily for 10 days to induce gastric carcinogenesis in rats. The effect of selenium on MNNG-induced gastric cancer in Wistar rats was observed on the 43th day of the experiment. The expression of p53 and p16 protein in this process was studied by immunohistochemical SP method And its changes, and the above results were qualitative, positioning, image analysis and statistical processing. Results The addition of 2 mg / L and 4 mg / L sodium selenite to drinking water aggravated gastric mucosal erosion and hemorrhage, and promoted intestinal metaplasia of gastric mucosa (P <0.05). Submucosal smoothing occurred during the induction of MNNG Fibroids, sodium selenite can increase the incidence of leiomyoma. The results of immunohistochemistry showed that the positive products of p53 were localized in the nucleus and cytoplasm, mainly in the cytoplasm. The average optical density (MA) of p53 protein in the experimental control group, low-selenium group and high-selenium group was significantly higher than that in the normal control group (P <0.05, P <0.01). The positive expression of p16 protein was observed in the rat gastric gland and gastric epithelial cells. The MA values in experimental control group, low selenium group and high selenium group were slightly higher than those in normal control group (P> 0.05). Conclusion In the course of gastric cancer induced by MNNG, adding 2mg / L, 4mg / L sodium selenite in drinking water can promote gastric mucosal erosion, hemorrhage and intestinal metaplasia, suggesting that sodium selenite does not reduce gastric cancer in rats The mechanism may be related to the aberrant expression of p16 and the mutation of tumor suppressor gene p53.