孙媛媛,敦云楼,胡婷,等.褐藻胶寡糖对刀豆蛋白A诱导的急性肝损伤保护作用及机制初探[J].中国海洋药物,2017,36(1):34-40.
褐藻胶寡糖对刀豆蛋白A诱导的急性肝损伤保护作用及机制初探
Study on hepatoprotective effects of alginate oligosaccharides on ConcanavalinA-induced acute liver injury
投稿时间:2016-05-06  修订日期:2016-06-22
DOI:
中文关键词:  褐藻胶寡糖,刀豆蛋白A,肝损伤
English Keywords:alginate oligosaccharides,Concanavalin A,liver injury
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作者单位E-mail
孙媛媛 海洋药物教育部重点实验室 sunyuanyuan@ouc.edu.cn 
敦云楼 中国海洋大学医药学院  
胡婷 青岛海洋生物医药研究院  
管华诗 中国海洋大学医药学院  
蔡兵 青岛海洋生物医药研究院  
郝杰杰* 中国海洋大学医药学院  
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中文摘要:
      目的 研究褐藻胶寡糖对刀豆蛋白A (Concanavalin A, ConA)诱导急性肝损伤的保护作用及其可能的作用机制。方法 本实验以分子量为3kDa的甘露糖醛酸寡糖(M-3k)和古罗糖醛酸寡糖(G-3k)为受试样品,通过检测ConA注射后14h血清转氨酶水平及肝组织病理学评估肝脏损伤;通过酶联免疫法(ELISA) 检测TNF-α、IL-6水平;Western Blotting法检测Bcl-2、Bax蛋白表达。结果 与模型组相比,褐藻胶寡糖预防组显著降低了ConA急性肝损伤小鼠血清AST和ALT水平(P<0.05),且组织病理学观察发现,肝细胞损伤、炎性浸润和凋亡程度减轻;与模型组相比,褐藻胶寡糖预防组显著降低了肝组织匀浆中促炎因子TNF-α、IL-6水平(P<0.05);褐藻胶寡糖预防组Bcl-2蛋白表达明显高于模型组(P<0.05),Bax蛋白表达水平明显低于模型组(P<0.05)。讨论 说明褐藻胶寡糖对ConA诱导小鼠急性肝损伤具有一定保护作用,并且其作用机制可能部分与抑制肝脏炎症反应和干扰凋亡过程有关。
English Summary:
      Objective To investigate the hepatoprotective effects of alginate oligosaccharides (AOS) on Concanavalin A(ConA) treated mice and the potential molecular mechanisms of that action. Methods The liver injury was examined by measuring serum Aspartate transaminase (AST) and Alanine aminotransferase (ALT) 14h after ConA injection, and was evaluated via histopathological observation. The levels of proinflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in liver tissue were determined by enzyme linked immunosorbent assay (ELISA). The expression of apoptosis factors Bcl-2 and Bax were detected by Western blotting. Results Compared with model group, AOS-pretreatment effectively reduced the elevated the levels of AST and ALT in plasma (P<0.05) , and liver histology analysis showed less hepatocellular injury, inflammatory infiltration and cell apoptosis. The levels of TNF-α and IL-6 in liver tissue were dramatically decreased by pretreatment of AOS compared to the model group (P<0.05) . The expression levels of Bcl-2 in liver tissue was obviously up-regulated by AOS, and the expression levels of Bax was down-regulated contrast to the model group (P<0.05) . Conclution AOS pretreatment protects against ConA-induced acute liver injury in mice, and the inhibition to ConA-induced liver damage in AOS-pretreated group is due partly at least to its anti-inflammatory activty and anti-apoptotic activity represented by their mediating in the expression of Bcl-2 and Bax.
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