摘要
从健康孕妇水囊引产4～6月龄的胎儿取肝,按 LaBrecque 法提取人肝刺激因子(hHSS)。将 hHSS 注入切除34%肝的 SD 大鼠腹腔,用~3H—胸腺嘧啶掺入肝 DNA 法,证实所提取 hHSS 具有生物学活性。用半乳糖胺(D—Gal)给昆明种小鼠造成急性肝损害。观察 hHSS 对这种急性肝损伤动物的保护作用及其机制。结果如下:(1)hHSS 明显降低 D—Gal 中毒小鼠的死亡率。(2)hHSS 显著降低 D—Gal 引起的血清 CPT 和 GOT 升高的幅度。(3)预先给 hHSS,则 D—Gal 引起的肝组织形态变化均减弱或不出现。(4)电子显微镜检查,hHSS 处理后由 D—Gal 引起的一些细胞器的变化均减轻或不出现。(5)hHSS 明显降低 D—Gal 所引起肝组织丙二醛的含量,说明 hHSS 有抗脂质过氧化作用。(6)hHSS 能保证膜流动性正常和脆性正常。根据上述实验资料,肯定了人肝刺激因子的存在,hHSS 具有保肝作用,其保肝机制为 hHSS 可抗膜脂质过氧化,保护肝细胞质膜、线粒体膜和微粒体膜的流动性和正常脆性。人胎肝产生 hHSS,hHSS 又可以保护肝细胞,这一肝细胞自我保护物质及其机制的阐明,对肝炎的防治可能具有应用价值。
hHSS was extracted from fetal liver of 4-6 months gastation according to the method of LaBreque.The stimulatory activity of hHSS was by specific incorporation rate of ~3H-thymindine on 34% hepatoctomy.The mice were injected with D-galactosamine to induce acute hepatic failure. The underlying mechanism of this effect was investigated with the following result:(1) The mortality induced by D-galactosamine could be reduced by hHSS;(2) The high level of sGPT and sGOT in D-gala- ctosamine-intoxicated mice could be lowed by hHSS;(3) hHSS could improved the hepatic lesions induced by D-galactosamine on light micro- scope;(4) hepatic histological findings on electron microscopic exami- nation indicate that the cells lesions can be improved by hHSS;(5) hHSS could decrease the liver malonaldehyde content of D-galactosamine- intoxicated mice;(6) hHSS have protection of maintaining the normal level of hepatic cytoplasm and membrane fludity to recover.According to the results mentioned above,we conclude that there are hHSS in fatal liver and it has hepatic protective effect and its mechanism could be inhibition of lipid peroxidation,maintenance of normal metabolism and membrane fluidity of liver cells.
关键词
人肝刺激因子
半乳糖胺
肝保护
human hepatic stimulator substancc
D-galactosamine
liver protectton
