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Fucoidan ameliorates steatohepatitis and insulin resistance by suppressing oxidative stress and inflammatory cytokines in experimental non-alcoholic fatty liver disease

机译:Fucoidan通过抑制实验性非酒精性脂肪肝疾病中的氧化应激和炎性细胞因子来改善脂肪性肝炎和胰岛素抵抗

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摘要

Fucoidan, a sulfated polysaccharide derived from brown seaweeds, possesses a wide range of pharmacological properties. In the present study, we investigated the therapeutic effect of fucoidan on non-alcoholic fatty liver disease (NAFLD) in rats. Rats were fed a high-fat diet (HFD) for 12 weeks to induce NAFLD. Oral administrations of fucoidan (100mg/kg, orally), metformin (200mg/kg, orally) or the vehicle were started in the last four weeks. Results showed that administration of fucoidan for 4 weeks attenuated the development of NAFLD as evidenced by the significant decrease in liver index, serum liver enzymes activities, serum total cholesterol and triglycerides, fasting serum glucose, insulin, insulin resistance, and body composition index. Further, fucoidan decreased hepatic malondialdehyde as well as nitric oxide concentrations, and concomitantly increased hepatic reduced glutathione level. In addition, the effect of fucoidan was accompanied with significant decrease in hepatic mRNA expressions of tumor necrosis factor-α, interleukins-1β and matrix metalloproteinase-2. Furthermore, histopathological examination confirmed the effect of fucoidan. In conclusion, fucoidan ameliorated the development of HFD-induced NAFLD in rats that may be, at least partly, related to its hypolipidemic, insulin sensitizing, antioxidant and anti-inflammatory mechanisms.
机译:岩藻依聚糖,一种衍生自褐藻的硫酸化多糖,具有广泛的药理特性。在本研究中,我们调查了岩藻依聚糖对大鼠非酒精性脂肪性肝病(NAFLD)的治疗作用。给大鼠喂食高脂饮食(HFD)12周,以诱导NAFLD。在过去四周内开始口服岩藻依聚糖(100 mg / kg,口服),二甲双胍(200mg / kg,口服)或赋形剂。结果显示,给予岩藻依聚糖4周可减缓NAFLD的发生,肝指数,血清肝酶活性,血清总胆固醇和甘油三酸酯,空腹血糖,胰岛素,胰岛素抵抗和身体组成指数均显着降低。此外,岩藻依聚糖降低了肝脏丙二醛和一氧化氮的浓度,并随之增加了肝脏降低的谷胱甘肽水平。此外,岩藻依聚糖的作用伴随着肿瘤坏死因子-α,白介素-1β和基质金属蛋白酶-2的肝mRNA表达的显着降低。此外,组织病理学检查证实了岩藻依聚糖的作用。总之,岩藻依聚糖改善了HFD诱导的大鼠NAFLD的发展,这可能至少部分与其降血脂,胰岛素增敏,抗氧化剂和抗炎机制有关。

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