论文部分内容阅读
本实验应用D—氨基半乳糖诱发大白鼠急性肝坏死模型,检测了实验动物的血浆肿瘤坏死因子(Tumor Nectosis,TNF)的含量、转氨酶和肝组织过氧化物水平(LOP);观察了肝坏死的表现及其与促肝细胞生长素(Hepa tocyte Growth-Promoting Factor HGF)保护组相比较。结果实验肝坏死动物血浆TNF含量和LPO水平明显升高,在用药24~48小时之间达高峰;肝病理为点、片状或亚大块坏死;而HGF保护的大鼠血浆THF含量与LPO显著低于非保护组(P<0.01,P<0.05),肝组织仅见少数肝细胞坏死。因此,肿瘤坏死因子是急性肝坏死的重要介质,而HGF对保护肝细胞,缓解肝坏死有一定作用。
In this study, D-galactosamine-induced acute liver necrosis model in rats was used to detect the levels of plasma Tumor Necrosis Factor (TNF) and aminotransferase (ALT) and liver tissue peroxide (LOP) in experimental animals. Liver necrosis And compared with the protective group of Hepa tocyte Growth-Promoting Factor (HGF). Results The plasma levels of TNF and LPO in experimental hepatic necrosis animals were significantly increased and peaked between 24 and 48 hours after treatment. The liver pathology was spotted, patchy or sub-massive necrosis. However, the plasma concentrations of HGF- (P <0.01, P <0.05). Only a few hepatocytes were necrotic in liver tissue. Therefore, tumor necrosis factor is an important medium for acute liver necrosis, while HGF has some effect on protecting liver cells and relieving hepatic necrosis.