脾气虚胃溃疡大鼠胃黏膜生长抑素相关信号转导分子的变化  

CHANGES OF SOMATOSTATIN RELATED SIGNAL TRANSDUCTION MOLECULARS IN RAT GASTRIC MUCOSA OF SPLEEN DEFICIENCY SYNDROME COMBINED WITH GASTRIC ULCER

作　　者：杜娟[1] 王秀琴[1] 季凤清[1] 曾晓蓓[1] 尚宏伟[1] 孙海梅[1] 张立新[1] 

机构地区：[1]首都医科大学组织学胚胎学教研室,北京100069

出　　处：《解剖学报》2008年第6期894-900,共7页Acta Anatomica Sinica

基　　金：北京市中医药管理局科技发展基金资助项目(GG2003-11)

摘　　要：目的探讨生长抑素及其信号传递分子与脾气虚胃溃疡的发生及转归的关系。方法选用成年Wistar大鼠,雌、雄性各35只,建立脾气虚胃溃疡大鼠模型;运用HE染色、免疫组织化学分析、RT-PCR及免疫印迹法,分别观察胃黏膜的组织结构、生长抑素含量、2型生长抑素受体mRNA、细胞外信号传递激酶2(ERK2)表达的变化。结果脾气虚胃溃疡大鼠胃黏膜中,2型生长抑素的蛋白含量增加,生长抑素受体mRNA表达上调,(ERK2)表达下降。结论生长抑素信号传递途径中相关信号分子的变化可能是引起脾气虚胃溃疡发生的原因之一。Objective To investigate the role of somatostatin and related signal transduction molecules in the process of spleen deficiency syndrome combined with gastric ulcer. Methods Seventy adult male and female Wistar rats were selected to set up an animal model of spleen deficiency syndrome combined with gastric ulcer. Then immunohistoehemistry, reverse-transcript PCR, Western blotting and hematoxylin-eosin staining were used to detect the changes of somatostatin, somatostatin receptor 2 mRNA, excellular signal-regulated kinase 2 （ERK2） and histological structure of gastric mucosa respectively. Results In the gastric mucosa of spleen deficiency syndrome combined with gastric ulcer, the content of somatostatin increased and the mRNA of somatostatin receptor 2 increased, while the content of ERK2 decreased. Conclusion Somatostatin signal transduction pathway may probably play an important role in the onset of spleen deficiency combined with gastric ulcer.

关 键 词：脾气虚 胃溃疡 生长抑素 信号传递 免疫组织化学 反转录-聚合酶链反应 免疫印迹法 大鼠 

分 类 号：R322.81[医药卫生—人体解剖和组织胚胎学]