摘要
目的: 研究肿瘤坏死因子(TNF-α)在诱导急性肝坏死发生中的作用。方法: 利用D 氨基半乳糖和内毒素建立急性肝坏死动物模型,抗TNF -α IgG抗体进行阻断。观察死亡率,血清ALT和TNF -α含量及肝组织病理学变化。结果: 肝坏死组动物 9h死亡率达 60%,ALT水平从 6h起明显升高, 9h达高峰,TNF -α含量 2h为最高值,各时间点较其它组均有显著性差异 (P<0.01)。抗体组无死亡,且ALT水平明显降低,较肝坏死组有明显差异(P<0.01)。肝坏死组动物 9h出现肝细胞大块或亚大块出血性坏死,抗体组病变明显减轻。结论: TNF- α是急性肝坏死发生中重要的细胞因子,抗TNF- α IgG抗体可以阻断肝坏死的发生。
Objective: To study the effect of tumor necrosis factor-α (TNF-α) on acute liver necrosis induced in mice. Methods: Male Balb/c mice received D-Galactosamine and lipopolysaccharide to induce acute liver necrosis. Serum levels of alanine transaminase (ALT) and TNFα were determined. The liver tissues were fixed for histopathologic analysis. The difference with pretreatment by using anti-TNF-α antibody was studied. Results: The mortality rate of mice with acute liver necrosis reached 60% 9 hours after injection. The serum levels of ALT began to increase from the 6th hour, and reached maximum at the 9th hour. The concentration of TNF-α reached a maximal value at the 2nd hour.The levels of TNF-α at every time point were significantly increased than that of control group (P<0.01). The liver were induced with massive or submassive necrosis. But there were no death in mice with anti-TNF-antibody pretreatment. Serum levels of ALT were significantly reduced (P<0.01). The histologic analysis showed only spotty necrosis or focal necrosis. Conclusion: The TNF-α is a key cytokine that induces liver necrosis. The treatment with anti-TNF-antibody prevents the liver necrosis.
出处
《中国医科大学学报》
CAS
CSCD
北大核心
2005年第1期54-56,共3页
Journal of China Medical University
关键词
急性肝坏死
肿瘤坏死因子
内毒素
acute liver necrosis
tumor necrosis factor
lipopolysaccharide
