白介素－1β对大鼠应激性胃粘膜损伤的保护作用  

THE PROTECTIVE EFFECT OF IL-1β ON STRESS-INDUCED GASTRIC MUCOSAL DAMAGE IN RAT

作　　者：黄忠[1] 李铁[1] 于吉人[1] 马大龙[1] 

机构地区：[1]北京医科大学生理学系,北京医科大学免疫学系

出　　处：《生理学报》1995年第4期313-319,共7页Acta Physiologica Sinica

基　　金：国家自然科学基金

摘　　要：本工作观察了人重组白介素１β（ＩＬ－１β）对大鼠束缚冷冻应激造成的胃粘膜损伤的影响。外周给予ＩＬ－１β后能防止胃粘膜损伤的形成，呈剂量依从关系。ＩＬ－１片段１６３－１７１对应激性胃粘膜损伤无明显影响。但巯基物质耗竭剂Ｎ－乙烯顺丁烯二酰亚胺（Ｎ－ｅｔｈｙｌｍａｌｅｉｍｉｄｅ）能部分阻断ＩＬ－１β的作用。应激３ｈ后胃粘膜蛋白质和非蛋白质巯基含量明显降低，而ＩＬ－１β能防止巯基含量的下降。ＩＬ－１β也能减少应激造成的胃粘膜脂质过氧化产物丙二醛（ｍｏｌｏｎｄｉａｙｌｄｅｈｙｄｅ）的含量。提示ＩＬ－１β能明显减轻大鼠应激性胃粘膜损伤程度，其机制可能与胃粘膜内源性巯基物质有关。The effect of recombinant IL- 1β on stress-induced gastric mucosal lessions was studied in rats. Pretreatment with IL-1β prevented formation of gastric mucosal damage in a dose-dependent manner.IL-1 receptor antagonist peptide (IRAP) could totally reverse the protective effect of IL- 1β. IL-1 fragment peptide (163-171 ) had no effect on gastric ulcer formation in the experimental model, whereas sulfhydryl blocker N-ehtylmaleimide partially blocked the protective effect of IL-1β. The concentration of protein and noneprotein sulfhydryls in the gastric mucosa was significantly decreased 3 h after stress, and this decrease was partially prevented by IL- 1β.IL-1β also decreased the concentration of molondialdehyde (MDA) in the gastric mucosa after 3 h stress.The resuits suggest that IL- 1β could effectively lessen the degree of stress-induced gastric mucosal damage, due possibly to the production of endogenous sulfhydryl compounds in the gastric mucosa.

关 键 词：胃粘膜损伤 巯基物质 白细胞介素-1Β 

分 类 号：R392.11[医药卫生—免疫学] R573.02[医药卫生—基础医学]