| 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、200 mg/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7 d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、200 mg/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。 |
| 关键词: 蕨麻多糖 D-氨基半乳糖 肝损伤 |
| DOI：10.16781/j.0258-879x.2016.07.0916 |
| 投稿时间：2015-10-31修订日期：2016-01-19 |
| 基金项目:甘肃省自然科学基金（0710RJZA045，145RJZA043），中央高校基本科研业务费专项资金（Lzujbky-2012-194），兰州市科技计划项目（2011-2-45），兰州大学国家级大学生创新创业训练计划（201610730166）. |
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| Protective mechanism of Potentilla anserina polysaccharide on mice with D-galactosamine-induced acute liver injury |
| MIN Guang-tao1,WANG Li-jun2,DUAN Zhong-ping3,MIN Guang-ning2*,HE Zhi-yun4,WANG Yong-qiang2 |
(1. Department of General Surgery, The First Hospital of Lanzhou University, Lanzhou 730000, Gansu, China;
2. Department of Pharmacy, The First Hospital of Lanzhou University, Lanzhou 730000, Gansu, China;
3. Artificial Liver Center, Beijing Youan Hospital, Capital Medical University, Beijing 100069, China;
4. Department of Colorectal Surgery, The Second Hospital of Lanzhou University, Lanzhou 730000, Gansu, China
* Corresponding author) |
| 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, 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. |
| Key words: Potentilla anserina polysaccharide D-galactosamine liver injury |
