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目的:考察银杏提取物(GBE)与刺梨配伍制备复方银杏叶制剂(CGB)对肝损伤保护作用及其可能机制。方法:84只清洁级雄性小鼠随机分为空白对照组,模型组,GBE组,CGB高、中、低剂量组,联苯双酯组。分别ig给予GBE组(0.4 g.kg-1),CGB高、中、低剂量组(2.4,0.8,0.4 g.kg-1),联苯双酯组(0.15 g.kg-1)小鼠相应剂量的药物4周后,除空白对照组外余组均一次性ig给予白酒6 g.kg-1,6 h后测定小鼠血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)及肝匀浆甘油三酯(TG)、丙二醛(MDA)含量;体内用H2O2诱导人肝L02细胞造成氧化损伤,观察细胞ALT,AST水平及总抗氧化能力。结果:与模型组比较,CGB高、中剂量组对小鼠AST,ALT,TG均显著降低(P<0.05或P<0.01),且CGB高、低剂量组MDA较模型组降低显著(P<0.05)。在体外除CGB低剂量组与模型组比较,肝细胞中AST无显著性差异外,余给药组均可显著降低ALT,AST,并提高总抗氧化(TAOC)水平(P<0.05或P<0.01);且CGB高、中剂量组与单方GBE比较,降低ALT升高TAOC水平更为显著(P<0.01)。结论:复方银杏叶制剂可防护乙醇及H2O2所致的肝损伤,其作用可能与其协同抗氧化活性有关。
Objective: To investigate the protective effect of Ginkgo biloba extract (GBGB) combined with Rosa roxburghii on hepatic injury and its possible mechanism. Methods: Eighty-four clean male mice were randomly divided into blank control group, model group, GBE group, CGB high, medium and low dose groups and bifendate group. The rats in GBE group (0.4 g.kg-1), CGB high, middle and low dose groups (2.4, 0.8, 0.4 g.kg-1) and Bifendate group (0.15 g.kg- After 4 weeks, the serum ALT, AST (AST) of the mice were measured after a single dose of 6 g.kg-1, ) And liver homogenate triglyceride (TG) and malondialdehyde (MDA). The oxidative damage induced by H2O2 in human L02 cells was observed in vivo. The levels of ALT and AST and the total antioxidant capacity were observed. Results: The levels of AST, ALT and TG in high and middle dose CGB groups were significantly lower than those in model group (P <0.05 or P <0.01), and MDA in CGB high and low dose groups were significantly lower than those in model group (P < 0.05). Except CGB low dose group and model group, there was no significant difference in AST in hepatocytes except the CGB low dose group, and the other drug groups could significantly reduce ALT, AST and increase the total antioxidant capacity (TAOC) (P <0.05 or P < 0.01). Compared with unilateral GBE, high and medium dose CGB decreased the level of TAOC in ALT increased significantly (P <0.01). Conclusion: Ginkgo biloba preparation can prevent hepatic injury induced by ethanol and H2O2, which may be related to its synergistic anti-oxidative activity.