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.
出处
《生理学报》
CAS
CSCD
北大核心
1995年第4期313-319,共7页
Acta Physiologica Sinica
基金
国家自然科学基金
关键词
胃粘膜损伤
巯基物质
白细胞介素-1Β
IL-1β
stress
ulcerations
sulfhydryl compounds
molondialdehyde