乙酸性胃溃疡大鼠一氧化氮、内皮素及表皮生长因子受体相互关系研究  

Relationship among Nitric Oxide, Endothelin-1 and Epidermal Growth Factor Receptor in Rats with Acetic Acid-induced Chronic Gastric Ulcer

作　　者：陈绍斌[1] 肖凤仪[1] 李国成[2] 

机构地区：[1]湖北省随州市中心医院中医科,随州441300 [2]华中科技大学同济医学院附属同济医院中医科,武汉430030

出　　处：《中国中西医结合消化杂志》2002年第5期259-261,共3页Chinese Journal of Integrated Traditional and Western Medicine on Digestion

基　　金：国家中医药管理局科研基金资助项目 (No.95 B15 1)

摘　　要：目的 :探讨一氧化氮 (NO)、内皮素 (ET- 1)、表皮生长因子受体 (EGFR)在乙酸性慢性胃溃疡大鼠中的作用及相互关系。方法 :采用乙酸性慢性胃溃疡疾病模型 ,游标卡尺测定溃疡指数 ,硝酸还原酶法测定 NO含量 ,放射免疫法检测血浆 ET- 1含量 ,SABC免疫组织化学方法及图像分析观察 EGFR在溃疡周围粘膜的表达。结果 :左旋精氨酸 (L - Arg)组溃疡指数与模型组及亚硝基左旋精氨酸 (L - NNA )组比较显差有显著性意义 (P <0 .0 5 ,<0 .0 1) ;L- Arg组血清 NO及血浆 ET- 1含量与对照组、模型组及 L- NNA组比较差异有显著性意义 (P <0 .0 5 ,<0 .0 1) ;L - NNA组血清 NO及血浆 ET- 1含量与模型组及对照组比较差异均有非常显著性意义 (均 P <0 .0 1) ;L -Arg组 EGFR表达较模型组、L- NNA组及对照组显著增加 (积分光密度值及阳性细胞占总面积百分比均 P <0 .0 5 ) ;L- NNA组 EGFR显著弱于模型组 (P<0 .0 1)。结论 :NO前体 L- Arg可以诱导、促进 NO合成 ,反馈性地抑制 ET- 1的释放 ,从而维持 NO和 ET的动态平衡及胃粘膜 EGFR正常水平表达 ,促进溃疡愈合。Objective: To investigate the roles of nitric oxide (NO), endothelin (ET 1) and epidermal growth factor receptor (EGFR) in rats with acetic acid induced chronic gastric ulcer and the interaction. Methods: The rat model was induced by acetic acid. The index of ulcer (UI) was measured by using a vernier. The level of NO was determined by the method of nitric acid reductase, and the plasma ET 1 level was detected by radioimmunoassay. The expression of EGFR in the mucosa around the ulcer was observed by SABC kit immunohistochemical method and MPIAS micro image analysis system.Results: (1) There was obvious difference in UI between L Arg group and control group, as well as between L Arg group and L NNA group (P< 0.05 , P< 0.01 respectively); (2) Obvious difference was found in the level of serum NO and plasma endothelin 1 between L Arg group and control group (P< 0.05 ), between L Arg group and model group (P< 0.01 ), and between L Arg group and L NNA group (P< 0.01 ). The levels of serum NO and plasma endothelin 1 in L NNA group was remarkably different from those in model group and control group (both P< 0.01 ): (3) The expression of EGFR in L Arg group was obviously increased as compared with that in model group (P< 0.05 ), L NNA group (P< 0.01 ) and control group (P< 0.01 ) respectively. The expression of EGFR in L NNA group was obviously weaker that in model group (P< 0.05 ). Conclusion: L Arg could inhibit the release of ET 1 and increase the expression of EGFR by inducing NO synthesis. As a result, it improved the healing of gastric ulcer and protected gastric mucosa.

关 键 词：胃溃疡 一氧化氮 内皮素 表皮生长因子受体 免疫组织化学 硝酸还原酶法 放射免疫法 动物模型 免疫组织化学 

分 类 号：R573.1[医药卫生—消化系统]