TNF-α参与消炎痛诱导大鼠胃粘膜损伤机制的探讨  

A study of tumor necrosis factor-α involvement in the pathogenesis of gastric mucosal injury induced by indomethacin in rats

作　　者：李国平[1] 邓长生[2] 杜意平[2] 黄梅芳[2] 郑文 

机构地区：[1]汕头大学医学院第二附属医院内科,汕头515041 [2]湖北医科大学第二医院消化内科,武汉430071

出　　处：《中国病理生理杂志》1999年第9期814-816,共3页Chinese Journal of Pathophysiology

摘　　要：目的：探讨消炎痛诱导大鼠胃粘膜损伤与血浆TNF－α活性的关系。方法与结果：随着消炎痛灌胃剂量的加大，胃粘膜损伤程度、中性粒细胞浸润程度、脂质过氧化程度加重，血浆TNF-α活性升高。预先给予对TNF－α单克隆抗体在抑制20mg/kg消炎痛诱导的血浆TNF－α活性升高，同时胃粘膜损伤程度及中性粒细胞浸润程度下降，但粘膜脂质过氧化改变不明显。结论：在消炎痛损伤胃粘膜过程中血浆TNF－α活性升高，INF－α可能与中性粒细胞的激活、促进其浸润至冒粘膜组织有关。拮抗TNF－α可减轻由消炎痛诱导的实验性胃粘膜损伤。AIM:To investigate the relations of gastric mucosal injury by indomethacin and plasm TNF -α activity in rats. METHODS and RESULTS: Leukocyte infiltraion, lipid peroxidation, plasma TNF - α activity were increased with the dosage of indomethacin administration. Pretreatment with McAb - TNF - α produced a significant improvement in damage, leukocyte infiltration when compared with pretrcatment with placebo in administration of indomethacin 20 mg/kg. In addition, the activity of TNF - α was reduced significantly, however lipid peroxidation was not changed significantly. CONCLUSIONS:TNF -α which activates leukocyte, stimulates the infiltration of leukocyte may involve the pathogenesis of indomethacin induced gastric mucosal injury. Neutralization of TNF -α ameliorates acute experimental gastric mucosal injury induced by indomethacin in rats.

关 键 词：消炎痛 肿瘤坏死因子 胃粘膜 大鼠 

分 类 号：R573.02[医药卫生—消化系统] R971.1[医药卫生—内科学]