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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。
Objective: To investigate the relationship between indomethacin-induced gastric mucosal injury and plasma TNF-α activity in rats. Methods and Results: With the increase of dosages of indomethacin, the degree of gastric mucosal injury, the degree of neutrophil infiltration, the degree of lipid peroxidation increased and the activity of plasma TNF-α increased. Pretreatment of TNF-α monoclonal antibody in inhibiting 20mg / kg indomethacin-induced plasma TNF-α activity increased, while the degree of gastric mucosal injury and neutrophil infiltration decreased, but no significant change in mucosal lipid peroxidation. CONCLUSION: In the process of indomethacin injury of gastric mucosa, the activity of plasma TNF-α is increased. INF-α may be related to the activation of neutrophils and the infiltration of mucosa. Antagonism of TNF- [alpha] reduces experimental gastric mucosal injury induced by indomethacin.