论文部分内容阅读
目的: 初步探讨草棉花花瓣提取物总黄酮(FGF)对大、小鼠急性实验性肝损伤的影响。方法: 用D GalN(400 mg/kg)及CCl4(50%橄榄油溶液,5 ml/kg)对大鼠进行攻击;用大剂量PAR(200 mg/kg)对小鼠进行攻击,分别建立3种急性实验性肝损伤模型,观察FGF对大、小鼠血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、肝组织超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量以及肝组织病理变化等指标的影响。结果:发现FGF对D GalN引起的肝损伤模型(400 mg/kg×7 d)的ALT虽比模型组低,但差异无统计学意义(P>0.05);FGF (800mg/kg×7 d)使ALT明显降低,与模型组相比,差异有统计学意义(P<0.01);FGF(400、800 mg/kg)使AST均明显降低,差异有统计学意义(P<0.01);FGF两个剂量组均使MDA的含量降低。FGF两个剂量组(400、800 mg/kg)对CCl4 引起的肝损伤模型均使血清ALT、AST水平明显降低,并能提高肝组织SOD活性,降低MDA含量。FGF(800、1 200 mg/kg)对PAR引起的肝损伤模型均使血清ALT、AST水平明显降低,并能提高肝组织SOD活性,降低MDA含量。在3种模型中FGF均能明显改善肝组织病理损伤程度。结论:FGF对大、小鼠3 种化学性肝损伤有明显的保护作用,其机制可能与FGF的抗氧化作用有关。
Objective: To investigate the effect of total flavonoids (FGF) extracted from petal cotton petals on acute experimental liver injury in mice. METHODS: Rats were challenged with D GalN (400 mg/kg) and CCl4 (50% olive oil solution, 5 ml/kg); mice were challenged with large doses of PAR (200 mg/kg) to establish 3 An acute experimental liver injury model was used to observe serum glutamate aminotransferase (ALT), aspartate aminotransferase (AST), liver tissue superoxide dismutase (SOD) activity, malondialdehyde (MDA) content, and liver in large and small mice. Histopathological changes and other indicators. RESULTS: The ALT in the liver injury model induced by FGF in D GalN (400 mg/kg×7 d) was lower than that in the model group, but the difference was not statistically significant (P>0.05); FGF (800 mg/kg×7 d) The ALT was significantly reduced, compared with the model group, the difference was statistically significant (P<0.01); FGF (400, 800 mg/kg) reduced the AST significantly, the difference was statistically significant (P<0.01); FGF two Each dose group reduced the MDA content. The FGF two-dose group (400,800 mg/kg) caused a significant decrease in serum ALT and AST levels in the liver injury model induced by CCl4, and increased SOD activity and decreased MDA content in the liver. FGF (800, 1 200 mg/kg) in the liver injury model induced by PAR can significantly reduce serum ALT, AST levels, and can increase SOD activity in the liver and reduce MDA content. In all three models, FGF could significantly improve the degree of liver pathological damage. Conclusion: FGF has obvious protective effects on three kinds of chemical liver injury in mice and mice. The mechanism may be related to the antioxidation of FGF.