Holothuria leucospilota polysaccharides alleviate liver injury via AMPK and NF-Kappa B signaling pathways in type 2 diabetic rats
文献类型： 外文期刊
作者： Zhao, Fuqiang 1 ; Zhu, Kexue 2 ; Zhao, Qiancheng 3 ; Liu, Qibing 5 ; Cao, Jun 1 ; Xia, Guanghua 1 ; Liu, Zhongyuan 1 ; Li 1 ;
作者机构： 1.Hainan Univ, Sch Food Sci & Engn, Hainan Engn Res Ctr Aquat Resources Efficient Uti, Haikou 570228, Hainan, Peoples R China
2.Chinese Acad Trop Agr Sci, Spice & Beverage Res Inst, Wanning 571533, Hainan, Peoples R China
3.Dalian Ocean Univ, Coll Food Sci & Engn, Dalian 116023, Peoples R China
4.Dalian Polytech Univ, Natl Engn Res Ctr Seafood, Collaborat Innovat Ctr Seafood Deep Proc, Dalian 116034, Peoples R China
5.Hainan Med Univ, Sch Basic Med & Life Sci, Haikou 571199, Hainan, Peoples R China
关键词： Holothuria leucospilota; Polysaccharide; Type 2 diabetes mellitus; Liver injury; Oxidative stress; Inflammation
期刊名称：JOURNAL OF FUNCTIONAL FOODS （ 影响因子：4.451； 五年影响因子：4.908 ）
ISSN： 1756-4646
年卷期： 2021 年 85 卷
页码：
收录情况： SCI
摘要： The study evaluated the beneficial effects of orally administered Holothuria leucospilota polysaccharides (HLP) on liver injury in diabetic rats. The results showed that HLP regulated liver glycogen, glycosylated serum protein, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. Simultaneously, HLP significantly reduced lipid accumulation in livers of diabetic rats (P < 0.05). In addition, HLP exerted anti-oxidant and antiinflammatory activities, together with repaired histological impairment of liver in diabetes. Moreover, HLP downregulated the mRNA and protein expression of inhibitors of nuclear factor kappa B kinase beta (IKK beta), nuclear factor kappa B P65 (NF-kappa B P65) and glycogen synthase kinase 3 beta (GSK3 beta), while upregulated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1) and AMP-activated protein kinase alpha (AMPK alpha) in the liver. These findings suggested that HLP improved liver injury via AMPK and NF-kappa B related signaling pathways in type 2 diabetic rats.
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