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Aqueous Extracts of Se-Enriched Auricularia auricular Exhibits Antioxidant Capacity and Attenuate Liver Damage in High-Fat Diet/Streptozotocin-Induced Diabetic Mice

氧化应激 丙二醛 糖基化 链脲佐菌素 抗氧化剂 谷胱甘肽过氧化物酶 超氧化物歧化酶 药理学 内科学 脂质过氧化 内分泌学 糖尿病 化学 医学 生物化学
作者
Chunyan Wei,Jingjing Wang,Cuicui Duan,Huimei Fan,Xiaoxiao Liu
出处
期刊:Journal of Medicinal Food [Mary Ann Liebert, Inc.]
卷期号:23 (2): 153-160 被引量:7
标识
DOI:10.1089/jmf.2019.4416
摘要

Oxidative stress triggered by hyperglycemia is thought to be a major factor in the development of liver disease during diabetes mellitus (DM). The aim of this study was to determine the antioxidant capacity of aqueous extracts of selenium-enriched Auricularia auricular (AESA) and further investigate the hepatic protection and potential mechanism of AESA in a mouse model of diabetes. An in vitro antioxidant assay confirmed that AESA exhibited better antioxidant capacity characterized by increased reducing power and scavenging capacity of free radicals, such as diphenyl picrylhydrazyl radical, hydroxyl radical, and superoxide radical. The diabetic model was induced by high-fat diet combined with a single injection of streptozotocin in C57BL/6 mice. Our results showed that AESA treatment improved diabetes-induced disorders of lipid metabolisms and alleviated liver damage in diabetic mice. Furthermore, the antioxidant enzyme activities of glutathione peroxidase and catalase in liver were increased and malondialdehyde level was decreased with AESA treatment compared with those in the DM group. In parallel, AESA significantly reduced the contents of tumor necrosis factor-alpha and interleukin-1beta in liver in comparison with the DM group. In addition, western blot results showed that the expression of receptor for advanced glycation end products (RAGE), phospho-c-Jun NH2-terminal kinase, phospho-extracellular signal-regulated kinase, and phospho-p38 kinase were remarkably decreased in AESA treatment group compared with DM group. Taken together, supplementation of AESA may effectively attenuate diabetic hepatopathology by exerting antioxidant function through the RAGE/mitogen-activated protein kinase pathway.
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