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本实验从脂质过氧化的角度对D-氨基半乳糖(Galn)诱导肝损伤的机理进行了观察和探讨,并通过体内和体外实验研究了锌对该种肝损伤的保护作用及其机理,实验结果显示,有关自由基代谢和脂质过氧化的几项指标在Galn处理的大鼠体内均发生明显变化,其变化规律基本与四氯化碳处理大鼠体内变化一致,这就提示,自由基诱导的脂质过氧化可能是Galn诱导肝损伤的主要原因之一。 对Galn诱导肝损伤大鼠进行预补锌实验表明,醋酸锌im 50mg Zn·kg~1,d~1×5 d,可以维持大鼠体内锌的水平,降低大鼠中毒死亡率,减轻肝脏组织病理变化,抑制脂质过氧化,促进蛋白质合成并改善肝脏功能,体外实验表明,补锌可以减少Galn染毒游离肝细胞的中毒死亡数,降低培养液中丙二醛浓度并维持还原型谷胱甘肽水平,由此证明,锌对肝损伤具有明显的保护作用,该作用是通过抗氧化和促进蛋白质合成来进行的。
In this experiment, the mechanism of liver injury induced by D-galactosamine (Galn) was observed and discussed from the perspective of lipid peroxidation. The protective effect and mechanism of zinc on liver injury were studied in vitro and in vivo. The experimental results show that several indicators of free radical metabolism and lipid peroxidation in Galn-treated rats have significant changes in the body, the change of the basic and carbon tetrachloride-treated rats in vivo changes, suggesting that freedom Base-induced lipid peroxidation may be one of the major causes of Galn-induced liver injury. Pretreatment with Galn induced liver injury rats showed that zinc acetate im 50mg Zn · kg ~ 1, d ~ 1 × 5d, can maintain the level of zinc in rats, reduce the mortality of rat poisoning, reduce the liver tissue Pathological changes, inhibition of lipid peroxidation, and promote protein synthesis and improve liver function in vitro experiments show that zinc can reduce Galn poisoning death of free hepatocytes, reduce the concentration of malondialdehyde in culture medium and maintain reduced glutathione Thus, it is demonstrated that zinc has a significant protective effect on liver injury through antioxidation and protein synthesis.