【摘要】 目的考察蕨麻多糖(PAP)对D-氨基半乳糖(D-GlaN)诱导的急性肝损伤小鼠肝脏的保护作用机制。方法 60只昆明小鼠随机分为正常对照组、模型对照组、联苯双酯组(阳性对照)以及PAP 50、100、200mg/kg各剂量组,每组10只。先分别给予生理盐水、联苯双酯以及不同剂量受试药PAP,然后除正常对照组注射生理盐水外,其余5组均于给药7d后用8%D-GlaN腹腔注射,建立D-GlaN急性肝损伤模型。24h后处死,测定小鼠肝组织中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)、谷胱甘肽(GSH)等指标。结果模型对照组小鼠肝组织中的MDA含量升高,SOD和GSH-Px活性降低,GSH含量降低,与正常对照组比较差异有统计学意义(P<0.05,P<0.01);联苯双酯以及50、100、200mg/kg各剂量PAP均可明显降低D-GlaN急性肝损伤小鼠肝组织中的MDA含量,提高SOD和GSH-Px的活性,增加GSH含量,与模型对照组相比差异有统计学意义(P<0.05,P<0.01)。结论 PAP对D-GlaN急性肝损伤小鼠肝脏的保护作用可能与其清除自由基、保护细胞膜和抗脂质过氧化有关。更多还原

【Abstract】 Objective To explore the protective mechanism of Potentilla anserina polysaccharide(PAP)on acute liver injury induced by D-galactosamine(D-GlaN)in mice.Methods Sixty Kunming mice were randomly divided into normal control group,model group,bifendate group(positive control)and PAP(50,100,200mg/kg)treated groups,with 10 mice in each group.After treatment with normal saline,bifendate and PAP(50,100,200mg/kg)for 7days,the mice in normal control group were injected intraperitoneally with normal saline,and those in the other 5groups were injected intraperitoneally with D-GlaN to establish acute liver injury models.All the animals were sacrificed 24 hafter model establishment,and the levels of hepatic superoxide dismutase(SOD),malondialdehyde(MDA),glutathione(GSH),and glutathione peroxidase(GSH-Px)were determined.Results Compared with normal control group,the model group had significantly increased hepatic MDA level(P<0.05)and significantly decreased activities of hepatic SOD,GSH-Px and level of GSH(P<0.05,P<0.01).Comparedwith the model group,bifendate and 50,100,200mg/kg PAP significantly decreased hepatic MDA level(P<0.05),increased the activities of hepatic SOD,GSH-Px and level of GSH(P<0.05,P<0.01)in mouse acute liver injury model.Conclusion PAP can protect the liver of mice with acute liver injury induced by D-GlaN,which is probably through scavenging free radicals,protecting cell membranes and inhibiting lipid peroxidation.更多还原