Key Laboratory of Molecular Animal Nutrition, Ministry of Education, College of Animal Science, Zhejiang University, Hangzhou 310058, China.
Mar Drugs. 2019 Nov 16;17(11):645. doi: 10.3390/md17110645.
Nonalcoholic fatty liver disease (NAFLD) has become the most common chronic liver disease closely associated with metabolic syndrome, but there are no validated pharmacological therapies. The aim of this study was to investigate the effect of chitosan oligosaccharide (COS) on NAFLD. Mice were fed either a control diet or a high-fat diet (HFD) with or without COS (200 or 400 mg/kg body weight (BW)) by oral gavage for seven weeks. Administration with COS significantly lowered serum lipid levels in the HFD-fed mice. The hepatic lipid accumulation was significantly decreased by COS, which was attributed to decreased expressions of lipogenic genes and increased expressions of fatty β-oxidation-related genes. Moreover, pro-inflammatory cytokines, neutrophils infiltration, and macrophage polarization were decreased by COS in the liver. Furthermore, COS ameliorated hepatic oxidative stress by activating the nuclear factor E2-related factor 2 (Nrf2) pathway and upregulating gene expressions of antioxidant enzymes. These beneficial effects were mediated by the activation of the adenosine monophosphate-activated protein kinase (AMPK) signaling pathway. Therefore, COS might be a potent dietary supplement to ameliorate NAFLD.
非酒精性脂肪性肝病（NAFLD）已成为与代谢综合征密切相关的最常见的慢性肝病，但目前尚无经过验证的药物治疗方法。本研究旨在探讨壳寡糖（COS）对 NAFLD 的影响。通过口服灌胃，将小鼠分别喂食对照饮食或高脂肪饮食（HFD），同时用或不用 COS（200 或 400mg/kg 体重）处理 7 周。COS 的给药显著降低了 HFD 喂养小鼠的血清脂质水平。COS 显著减少了肝内脂质堆积，这归因于脂肪生成基因表达的降低和脂肪酸β氧化相关基因表达的增加。此外，COS 通过减少肝脏中的促炎细胞因子、中性粒细胞浸润和巨噬细胞极化来发挥作用。此外，COS 通过激活核因子 E2 相关因子 2（Nrf2）通路和上调抗氧化酶的基因表达来改善肝氧化应激。这些有益作用是通过激活单磷酸腺苷激活的蛋白激酶（AMPK）信号通路来介导的。因此，COS 可能是一种有效的膳食补充剂，可改善 NAFLD。
