中文摘要：

目的观察过山蕨总黄酮对肝损伤的保护作用,探讨其可能的肝保护机制。方法采用CCl4致急性肝损伤小鼠模型、扑热息痛致急性肝损伤小鼠模型、地塞米松联合酒精致脂肪性肝损伤小鼠模型、ConA致免疫性肝损伤小鼠模型,考察过山蕨总黄酮的肝保护作用;并考察过山蕨总黄酮体外对H2O2损伤的人肝细胞L02的影响。结果过山蕨总黄酮对CCl4致急性肝损伤小鼠、扑热息痛致急性肝损伤小鼠、ConA致免疫性肝损伤小鼠及地塞米松联合酒精致脂肪性肝损伤小鼠均有降低血清丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）的作用,还可增加肝组织过氧化氢酶（CAT）、超氧化物歧化酶（SOD）的活性,降低肝组织丙二醛（MDA）、转化生长因子β1（TGF-β1）、组织金属蛋白酶抑制物（TIMP-1）及层黏连蛋白（LN）的量。过山蕨总黄酮对L02细胞H2O2损伤有抑制作用,可刺激肝细胞血红素氧化酶（HO-1）活性,抑制H2O2所致的细胞还原型谷胱甘肽（GSH）耗竭及乳酸脱氢酶（LDH）释放,对DPPH自由基的清除作用相当于维生素E的68.55%。结论过山蕨总黄酮对肝损伤有保护作用,其机制可能与清除自由基和增强细胞抗氧化功能有关。

英文摘要：

Objective To investigate the protective effect and possible mechanism of total flavonoids from Comptosorus sibiricus（TFCS） on hepatic injury（HI）.Methods The acute hepatic injury（AHI） in mice induced by carbon tetrachloride（CCl4） and Paracetamol,immunologic hepatic injury（IHI） induced by concanavalin A（ConA）,and fatty hepatic injury（FHI） induced by Dexamethasone combined with ethanol（DCE） were used to examine the protective effect of TFCS on hepatic injury.The effect of TFCS on the damage of human hepatic cell L02 induced by hydrogen peroxide（H2O2） was observed in vitro.Results TFCS showed a protective effect on mice with AHI induced by CCl4and Paracetamol,IHI induced by ConA,and FHI induced by DCE by decreasing the contents of alanine aminotransferase（ALT） and aspartate aminotransferase（AST） in serum,increasing the activities of catalase（CAT） and superoxide dismutase（SOD） in hepatic tissue,and decreasing the levels of malondialdehyde（MDA）,transforming growth factor-β1（TGF-β1）,tissue inhibitor of metalloproteinase-1（TIMP-1）,and laminin（LN） in hepatic tissue.TFCS prevented L02 cells from damaging induced by H2O2,stimulated the activity of heme oxygenase-1（HO-1） in liver cells,and inhibited the depletion of glutathione hormone（GSH） and the release of lactate dehydrogenase（LDH） induced by H2O2.The scavenging effect of TFCS on free radical caused by DPPH was equal to 68.55% of vitamin E.Conclusion TFCS has a protective effect on HI and its mechanism is probably related to the scavenging of free radical and increasing of cell anti-oxidative function.