食品科学 ›› 2023, Vol. 44 ›› Issue (3): 137-145.doi: 10.7506/spkx1002-6630-20220322-276

• 营养卫生 • 上一篇    下一篇

岩藻多糖对酒精暴露小鼠肝损伤的保护作用及机制

杨佳,党凯,薛美兰,梁惠,张楠,王青,裴忠仟,秦益民   

  1. (1.青岛大学基础医学院,山东?青岛 266071;2.青岛大学公共卫生学院,山东?青岛 266071;3.青岛大学附属医院眼科,山东?青岛 266021;4.青岛明月海藻集团有限公司,海藻生物活性物质国家重点实验室,山东?青岛 266555)
  • 出版日期:2023-02-15 发布日期:2023-02-28
  • 基金资助:
    国家自然科学基金面上项目(81872605);山东省自然科学基金项目(ZR2020MH215); 山东省重大科技创新项目(2019JZZY010818)

Protective Effect and Mechanism of Fucoidan on Alcohol-Induced Liver Injury in Mice

YANG Jia, DANG Kai, XUE Meilan, LIANG Hui, ZHANG Nan, WANG Qing, PEI Zhongqian, QIN Yimin   

  1. (1. School of Basic Medicine, Qingdao University, Qingdao 266071, China;2. School of Public Health, Qingdao University, Qingdao 266071, China; 3. Department of Ophthalmology, The Affiliated Hospital of Qingdao University, Qingdao 266021, China; 4. State Key Laboratory of Bioactive Seaweed Substances, Qingdao Brightmoon Seaweed Group Co., Ltd., Qingdao 266555, China)
  • Online:2023-02-15 Published:2023-02-28

摘要: 目的:探讨岩藻多糖对酒精性肝病(alcoholic liver disease,ALD)的保护效果及潜在的分子机制。方法:用体积分数50%乙醇溶液建立ALD小鼠模型,再给予300 mg/kg mb岩藻多糖干预,比较对照组、酒精模型组与岩藻多糖干预组的肝组织形态学变化,测定血清转氨酶活力、血脂5 项、炎性因子4 项水平及辅助性T细胞(helper T cell,Th)1、Th2和Th17的比例,自噬蛋白表达水平和微管相关蛋白1轻链3β(microtubule-associated protein 1 light chain 3 beta,LC3B)荧光蛋白表达水平等指标,探究岩藻多糖对ALD的改善机制。结果:岩藻多糖可改善肝组织的不良病理变化,降低小鼠血清转氨酶(谷丙转氨酶、谷草转氨酶(aspartate aminotransferase,AST))和血脂(甘油三酯、总胆固醇、低密度脂蛋白胆固醇、总胆汁酸)水平(P<0.05),降低血清炎性因子(肿瘤坏死因子-α、白细胞介素(interleukin,IL)-1β和IL-6)和炎性细胞Th1、Th2和Th17的比例(P<0.05),下调自噬蛋白p62、哺乳动物雷帕霉素靶蛋白复合体1和核糖体蛋白70S6激酶等蛋白表达(P<0.05),促进转录因子EB的核转位(P<0.05),上调LC3B II蛋白和LC3B荧光蛋白的表达(P<0.05)。结论:岩藻多糖可改善ALD小鼠肝脏脂质毒性和炎症损伤,其作用机制可能与激活自噬有关。

关键词: 自噬;酒精性肝病;岩藻多糖;血脂;炎症

Abstract: Objective: To investigate the protective effect and potential molecular mechanism of fucoidan on alcoholic liver injury. Methods: A mouse model of alcoholic liver disease (ALD) was established using 50% (V/V) alcohol, and then administered with 300 mg/kg mb of fucoidan. Liver histomorphological changes were compared in the control, ALD and fucoidan intervention groups, and the levels of serum aminotransferase, serum lipids, and inflammatory factors, the proportion of T helper (Th) cells including Th1, Th2 and Th17, and the expression levels of autophagy-related proteins and microtubule-associated protein 1 light chain 3 beta (LC3B) were detected to explore the mechanism by which fucoidan can improve alcoholic liver injury. Results: Fucoidan could improve the pathological changes of liver tissue, reduce the levels of serum alanine (aminotransferase (ALT) and aspartate aminotransferase (AST)) and blood lipids (triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and total bile acid (TBA)) (P < 0.05), and decrease the levels of serum inflammatory factors (TNF-α, IL-1β and IL-6) and the proportion of Th1, Th2 and Th17 (P < 0.05). Meanwhile, it could down-regulate the expression of autophagy-related protein p62, mammalian target of rapamycin complex 1 (mTORC1) and ribosomal protein 70S6 kinase (p70S6K) (P < 0.05), promote the nuclear translocation of transcription factor EB (TFEB) (P < 0.05), and up-regulate the expression of LC3B II protein and LC3B fluorescent protein (P < 0.05). Conclusion: Fucoidan can alleviate lipotoxicity and inflammatory injury in the liver of ALD mice, and its mechanism may be related to the activation of autophagy.

Key words: autophagy; ethanol-induced liver injury; fucoidan; blood lipids; inflammation

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