蕨麻多糖保护D-氨基半乳糖急性肝损伤小鼠的作用机制

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.24 h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.

Protective mechanism of Potentilla anserina polysaccharide on mice with D-galactosamine-induced acute liver injury

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, 200 mg/kg) treated groups, with 10 mice in each group. After treatment with normal saline, bifendate and PAP (50, 100, 200 mg/kg) for 7 days, the mice in normal control group were injected intraperitoneally with normal saline, and those in the other 5 groups were injected intraperitoneally with D-GlaN to establish acute liver injury models. All the animals were sacrificed 24 h after 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). Compared with the model group, bifendate and 50, 100, 200 mg/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.