摘要
为探讨TNF-α在刀豆蛋白A(ConA)诱导的肝损伤中的作用,在ConA诱导的小鼠急性肝损伤模型上,观察血浆TNF-α含量、ALT活性、光镜和电镜下肝组织病理变化及应用抗TNF-α单抗的肝损伤阻断作用。结果发现,与正常对照组比较,模型组TNF-α、ALT明显增高[分别为(0.19±0.06)ng/ml,(1414±567)U/L,均为P<0.01],肝损伤在光镜、电镜下表现为肝细胞凋亡和坏死;抗TNF-α单抗组的TNF-α、ALT分别较模型组和无关单抗组明显降低,未见肝细胞凋亡和坏死。结果表明:肝细胞凋亡可能为ConA诱导肝细胞死亡的机制;TNF-α在ConA性肝损伤模型中起重要的介导作用;抗TNF-α单抗可以阻断ConA性肝损伤的发生,即有肝细胞保护作用。
To study the effect of monoclonal anti-TNF-α antibody on the concanavalin (ConA) -induced liver injury, the changes in plasma levels of alanine aminotransferase (ALT), tumor necrosis factor-α (TNF- α) and histopathology by light and electron microscopy were observed in the model of acute liver injury in mice induced by ConA as well as the protective effect of monoclonal anti-TNF-α antibody against hepatic injury in- vestigated. The results showed that plasma TNF-α and ALT levels in the model group [ (0. 19±0.06) μg/L and (1414±567) U/L] were significantly higher than those in the control group (P<0.01). Hepatic injury was characterized by apoptosis and necrosis of hepatic cells; Plasma TNF-α and ALT levels in the monoclonal anti-TNF-α antibody group were significantly lower than those in the model group and the group of the insignif- icant monoclonal antibody. Pathologic examination gave no evidence for apoptosis and necrosis. These results indicated that apoptosis might be an important mechanism of liver cell death induced by ConA in vovo. TNF-α has an important effect on this model; Monoclonal anti-TNF-α antibody can prevent hepatic injury indued by ConA.
出处
《同济医科大学学报》
CSCD
2000年第6期513-514,共2页
Acta Universitatis Medicinae Tongji
关键词
肿瘤坏死因子
单克隆抗体
刀豆蛋白A
肝损伤
tumor necrosis factor
monoclonal antibody
concanavalin A
liver injury
apoptosis