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[目的]研究左卡尼汀(L-carnitine,LC)对小鼠和大鼠实验性肝损伤的保护作用和机制。[方法]复制四氯化碳(CCl4)所致急性和慢性肝损伤的动物模型(小鼠腹腔注射CCl4,大鼠皮下注射CCl4)。将受试动物随机分为正常对照组,CCl4模型组,LC组,硫普罗宁片(tiopronin tablets)对照组或水飞蓟片(legalon tablets)组。用酶生化法测定血清生化指标谷丙转氨酶(ALT)和谷草转氨酶(AST)的水平,总胆红素(T-BIL)、总蛋白(TP)、白蛋白(ALB)、白球比值(A/G),肝组织超氧化物岐化酶(SOD)、谷胱甘肽过氧化物酶(GSH-px)和抗超氧阴离子能力(A-ASC)的活性、总抗氧化能力(T-AOC)以及脂质过氧化产物丙二醛(MDA)的含量。同时计算肝系数(liverindex,LI),行慢性肝损伤组织病理学检查。[结果]经口给予各剂量LC(0.25-1.0g·kg-1)后急性肝损伤动物血清ALT、AST及LI均明显降低,呈现剂量依赖性(P﹤0.05,P﹤0.01),大鼠和小鼠肝组织内SOD、GSH-px、A-ASC的活性及T-AOC水平均升高(P﹤0.05,P﹤0.01),而MDA的含量随LC剂量的升高而降低(P﹤0.05,P﹤0.01)。0.15g·kg-1的LC能显著降低慢性肝损伤大鼠血清ALT、AST及LI、T-BIL(P﹤0.01),增加TP、ALB和A/G比值(P﹤0.01),并有效减轻大鼠肝组织病理性改变。[结论]LC对CCl4所致的动物急慢性肝损伤均具有保护作用,其机制与其抗氧化特性有关。
[Objective] To investigate the protective effect and mechanism of L-carnitine (LC) on experimental liver injury in mice and rats. [Method] The animal model of acute and chronic hepatic injury induced by carbon tetrachloride (CCl4) was duplicated (CCl4 intraperitoneal injection in mice and CCl4 subcutaneously in rats). The test animals were randomly divided into normal control group, CCl4 model group, LC group, tiopronin tablets control group or legalon tablets group. Serum biochemical parameters, such as ALT and AST, T-BIL, TP, ALB and A / G), activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-px) and anti-superoxide anion (A-ASC) ) And lipid peroxidation product malondialdehyde (MDA) content. At the same time, liver index (LI) was calculated and histopathological examination of chronic liver injury was performed. [Results] The serum levels of ALT, AST and LI in acute liver injury rats were significantly decreased after oral administration of LC (0.25-1.0g · kg-1) in a dose-dependent manner (P <0.05, P <0.01) (P <0.05, P <0.01), while the content of MDA decreased with the increase of LC dose (P < 0.05, P <0.01). The serum level of ALT, AST, LI, T-BIL and the ratio of TP, ALB and A / G of rats with chronic hepatic injury were significantly decreased by 0.15g · kg-1 LC (P <0.01) Rat liver histopathological changes. [Conclusion] LC has a protective effect on acute and chronic hepatic injury induced by CCl4, and its mechanism is related to its antioxidant properties.