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家兔输注内毒素0.3mg/kg复制内毒素休克模型。输注4hr以后PMN吞噬发光和O_2生成呈持续升高(P<0.05～0.01),同时激活的PMN释放氧自由基损伤肝细胞,引起肝细胞内MDA含量和培养上清LDH活性升高(P>0.05～0.01)。体外内毒素与PMN共孵,PMN吞噬发光和O_2生成呈先升高后回降的变化,经内毒素在体外激活的PMN也能明显引起肝细胞内MDA含量和上清LDH活性升高(P<0.01),SOD活性下降(P<0.05)。给予外源性SOD能部分抑制PMN对肝细胞的损伤作用。结果提示,无论是体外还是体内,内毒素均能激活PMN,引起PMN释放氧自由基导致肝细胞产生酯质过氧化反应,损伤肝细胞。预先给予SOD对上述损伤有一定的保护效应。
Rabbits implanted endotoxin 0.3mg / kg replicate endotoxic shock model. PMN phagocytosis and O 2 generation continued to increase after 4 hours of infusion (P <0.05-0.01). Meanwhile, activated PMN released oxygen free radicals to damage hepatocytes, resulting in the increase of MDA content and LDH activity in the culture supernatant (P > 0.05 ~ 0.01). In vitro, endotoxin was incubated with PMN, PMN phagocytosis and O 2 production first increased and then decreased, and PMN activated by endotoxin in vitro could also significantly increase the content of MDA and the activity of supernatant LDH (P <0.01), SOD activity decreased (P <0.05). Exogenous SOD can partially inhibit the damage of PMN to hepatocytes. The results suggest that endotoxin can activate PMN in both in vitro and in vivo, causing PMN to release oxygen free radicals, leading to peroxidation of liver cells and damage of hepatocytes. Pre-given SOD has some protective effect on the above damage.