Tang S G, Dong X J
Department of Infectious Diseases, Third Affiliated Hospital of China Medical University.
Zhonghua Nei Ke Za Zhi. 1993 Feb;32(2):97-9.
The activity of tumor necrosis factor (TNF) in serum and in peripheral blood monocytes (PBMC) was determined in 8 patients with fulminating viral hepatitis (FVH), 10 patients with chronic active hepatitis (CAH) and 10 health controls. The activity was monitored in FVH patients before and after treatment with hepatocyte growth factor (HGF). It was found that TNF level was significantly higher in CAH patients than in controls (t = 3.56, P < 0.01) and also significantly higher in FVH than in CAH patients (t = 3.07, P < 0.01). The activity of TNF decreased gradually in FVH patients after HGF treatment and there was a positive correlation (r = 0.09, P < 0.01) between the activity of serum and PBMC TNF. It was found that in animal models of hepatic necrosis there was transient elevation of TNF activity with its peak occurring after 6 hours; the peak could be lowered with HGF treatment (t = 3.65, P < 0.05). The authors are of the opinion that TNF is an important mediator causing hepatic necrosis. The relationship between HGF and TNF was also discussed.
对8例暴发性病毒性肝炎(FVH)患者、10例慢性活动性肝炎(CAH)患者和10名健康对照者测定了血清及外周血单核细胞(PBMC)中肿瘤坏死因子(TNF)的活性。在FVH患者接受肝细胞生长因子(HGF)治疗前后监测该活性。结果发现,CAH患者的TNF水平显著高于对照组(t = 3.56,P < 0.01),FVH患者的TNF水平也显著高于CAH患者(t = 3.07,P < 0.01)。FVH患者经HGF治疗后TNF活性逐渐降低,血清和PBMC中TNF活性之间存在正相关(r = 0.09,P < 0.01)。发现在肝坏死动物模型中,TNF活性有短暂升高,在6小时后达到峰值;HGF治疗可降低该峰值(t = 3.65,P < 0.05)。作者认为TNF是导致肝坏死的重要介质。还讨论了HGF与TNF之间的关系。