魏芬芬,王文娟,贺青华,张波.枸杞多糖对小鼠酒精性肝损伤的保护作用及机制研究[J].药物评价研究,2019,42(5):852-857
枸杞多糖对小鼠酒精性肝损伤的保护作用及机制研究
Protective mechanism of Lycium Barbarum Polysaccharide on alcohol-induced liver injury in mice
投稿时间:2018-11-16  
DOI:10.7501/j.issn.1674-6376.2019.05.008
中文关键词:  枸杞多糖;酒精性肝损伤;抗氧化;抗炎
英文关键词:Lycium barbarum polysaccharide;acute alcoholic liver injury;antioxidation;anti-inflammatory
基金项目:
作者单位E-mail
魏芬芬 北京联合大学生物活性物质与功能食品北京市重点实验室, 北京联合大学生物化学工程学院, 北京 100191  
王文娟 北京联合大学生物活性物质与功能食品北京市重点实验室, 北京联合大学生物化学工程学院, 北京 100191  
贺青华 北京联合大学生物活性物质与功能食品北京市重点实验室, 北京联合大学生物化学工程学院, 北京 100191  
张波 北京联合大学生物活性物质与功能食品北京市重点实验室, 北京联合大学生物化学工程学院, 北京 100191 zhangbo_wl@buu.edu.cn 
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中文摘要:
      目的 研究枸杞多糖对小鼠酒精性肝损伤的保护作用及机制。方法 将小鼠随机分为对照组、模型组和枸杞多糖低、中、高剂量(75、150、300 mg/kg)组,第1~9天于每日13:00时分别ig给药,模型组和对照组给予等量双蒸水。第10~16天给药4 h后,枸杞多糖和模型组小鼠均ig 50%酒精20 mL/kg进行造模,对照组小鼠给予等量双蒸水。观察小鼠一般状态,末次ig酒精16 h后处死小鼠,检测肝脏指数;全自动生化分析仪检测血清中丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、三酰甘油(TG)、总胆固醇(TC)水平;试剂盒法测定肝组织丙二醛(MDA)、还原型谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-Px)、总超氧化物歧化酶(SOD)及炎性因子肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)的含量;HE染色观察肝组织病理变化。结果 与模型组比较,枸杞多糖各剂量组小鼠醒酒时间短,毛色有所改善,较活跃;各剂量组肝脏指数呈下降趋势,但不具有统计学意义;各剂量组血清ALT、AST、TC、TG均呈下降趋势,其中高、中剂量组ALT显著降低(P<0.05),3个剂量组TG浓度均差异显著(P<0.01);各剂量组小鼠肝脏MDA含量显著降低(P<0.05、0.01),GSH、SOD水平显著升高(P<0.05、0.01),GSH-Px水平升高但未表现出显著性差异;高、中剂量组小鼠肝脏TNF-α和IL-1β水平显著降低(P<0.05、0.01)。HE染色显示,与模型组比较,枸杞多糖各组肝组织破坏程度较轻。结论 枸杞多糖对于乙醇诱导的酒精性肝损伤具有一定的保护作用,作用机制可能与通过清除体内多余自由基、增强体内抗氧化能力以及减轻炎症反应相关。
英文摘要:
      Objective To investigate the protection of lycium barbarum polysaccharide (LBP) on alcohol-induced liver injury and explore their pharmacological mechanisms.Methods 60 male mice were randomly divided into five groups, normal control group, model group and LBP different concentrations (75, 150, 300 mg/kg) groups. Drugs was ig administered at 13:00 a day on the 1st to 9th day. The model group and the control group were given the same amount of double steamed water. After 4 hours of administration from 10th to 16th day, alcoholic liver injury model was induced by 50% ethanol for 7 days. The general state of mice was observed. After 16 h of the last administration, serum and liver were obtained and related markers were determined. The liver tissue injury situation was assessed by HE staining. The levels of serum alanine transaminase (ALT), serum aspartate transaminase (AST), serum triglyceride (TG) and serum total cholesterol (TC), and the liver levels of malondialdehyde (MDA), glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and inflammatory factor TNF-α, IL-1β were measured. Results Compared with model group, LBP group had shorter sobering time, better hair color and more active; liver index of each dose group showed a downward trend, but not statistically significant; ALT, AST, TC and TG in serum of each dose group showed a downward trend, and ALT in high and middle dose groups decreased significantly (P<0.05), and TG concentration in three dose groups had significant difference (P<0.01); MDA content in liver of rats decreased significantly (P<0.05, 0.01), GSH and SOD levels increased significantly (P<0.05, 0.01), GSH-Px levels increased but there was no significant difference; TNF-α and IL-1β levels in liver of mice in high and medium dose groups decreased significantly (P<0.05, 0.01). HE staining showed that compared with the model group, LBP groups had less damage to liver tissue. Conclusion LBP have protective effect on alcohol-induced acute alcoholic liver injury, the mechanism may be related to the elimination of excess free radicals, the enhancement of antioxidant capacity and the alleviation of inflammation.
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