硒在早期实验性胃癌发生过程中诱导的组织学和超微结构变化。

Histological and ultrastructural changes induced by selenium in early experimental gastric carcinogenesis.

作者信息

Su Yan-Ping, Tang Jun-Min, Tang Yan, Gao Hui-Ying

机构信息

Department of Histology and Embryology, Taishan Medical College, Taian 271000, Shandong Province, China.

出版信息

World J Gastroenterol. 2005 Aug 7;11(29):4457-60. doi: 10.3748/wjg.v11.i29.4457.

DOI:10.3748/wjg.v11.i29.4457

PMID:16052671

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4398691/

Abstract

AIM

To investigate the effect and significance of selenium in early experimental gastric carcinogenesis.

METHODS

Weaning male Wistar rats were divided randomly into normal control group, experiment control group, low selenium (2 mg/L) group and high selenium (4 mg/L) group. Wistar rat gastric carcinogenesis was induced by N-methyl-N-nitro-N-nitroso guanidine (MNNG) (20 mg/kg) gavage daily for 10 d. Na2SeO3 was given by piped drinking 1 wk prior to MNNG gavage. The rats were killed at the 43rd wk. The surface characteristics of gastric mucosa were observed with naked eyes. Histopathologic changes of rat gastric mucosa were observed by HE staining and AB-PAS methods. The changes of cellular ultrastructure were observed under transmission electron microscope. Statistical analysis was carried out by SPSS.

RESULTS

The incidence rate of gastric mucosa erosion, hemorrhage and intestinal metaplasia was 0, 45.5%, 66.7%, and 92.9%, respectively (92.9% vs 45.5%, P < 0.05) in the normal control group, experiment control group, low selenium group, and high selenium group. Leiomyoma formed in the process of inducement of rat gastric carcinoma. Dietary Na2SeO3 (2 and 4 mg/L) slightly increased the incidence rate of leiomyoma (0, 23%, 46.6%, and 46.6%). gastric mucosa did not change in the course of rat gastric carcinogenesis. Dietary Na2SeO3 by pipe drinking could expand the intracellular secretory canaliculus of parietal cells and increase the number of endocrine cells and lysosomes.

CONCLUSION

Dietary Na2SeO3 by pipe drinking aggravates gastric erosion, hemorrhage and promotes intestinal metaplasia of gastric mucosa. The mechanism may be related with the function of parietal cells.

摘要

目的

探讨硒在早期实验性胃癌发生中的作用及意义。

方法

将断乳雄性Wistar大鼠随机分为正常对照组、实验对照组、低硒（2mg/L）组和高硒（4mg/L）组。采用N-甲基-N-硝基-N-亚硝基胍（MNNG）（20mg/kg）每日灌胃10天诱导Wistar大鼠胃癌发生。在MNNG灌胃前1周通过管道饮水给予亚硒酸钠。在第43周处死大鼠。肉眼观察胃黏膜的表面特征。采用苏木精-伊红（HE）染色和AB-PAS法观察大鼠胃黏膜的组织病理学变化。在透射电子显微镜下观察细胞超微结构的变化。采用SPSS进行统计学分析。

结果

正常对照组、实验对照组、低硒组和高硒组胃黏膜糜烂、出血和肠化生的发生率分别为0、45.5%、66.7%和92.9%（92.9%对45.5%，P<0.05）。在大鼠胃癌诱导过程中形成了平滑肌瘤。膳食亚硒酸钠（2mg/L和4mg/L）使平滑肌瘤的发生率略有增加（0、23%、46.6%和46.6%）。大鼠胃癌发生过程中胃黏膜无变化。通过管道饮水给予膳食亚硒酸钠可扩大壁细胞的细胞内分泌小管，并增加内分泌细胞和溶酶体的数量。