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梅花参岩藻聚糖硫酸酯对胰岛素抵抗小鼠慢性炎症的改善作用及其机制研究 被引量:3

The effect of fucoidan fromThelenota ananas on ameliorating chronic inflammation in insulin resistant mice
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摘要 目的研究梅花参岩藻聚糖硫酸酯(Fucoidan fromThelenota ananas,Ta-FUC)对高脂高果糖诱导的胰岛素抵抗模型小鼠慢性炎症的改善作用及相关信号通路。方法采用高脂高果糖饲喂C57BL/6小鼠,建立胰岛素抵抗模型。雄性C57BL/6小鼠随机分为6组:正常对照组、模型对照组、阳性对照组(RSG,1mg·(kg·d)-1)、Ta-FUC低剂量组(20mg·(kg·d)-1)和Ta-FUC高剂量组(80mg·(kg·d)-1)。连续饲喂13周后,检测各组小鼠血糖、胰岛素和炎症因子水平以及炎症信号通路NF-κB中关键基因mRNA的表达。结果Ta-FUC能显著降低小鼠体脂比,显著降低空腹血糖和空腹血清胰岛素水平,提高葡萄糖和胰岛素耐受水平。显著降低血清促炎因子FFA、TNF-α、IL-6、抵抗素、瘦素和CRP含量,显著提高血清抗炎因子IL-10和脂联素含量。显著下调NF-κB信号通路关键基因Ikkβ和NF-κB mRNA的表达量,上调NF-κB抑制物I-κBαmRNA的表达量。结论梅花参岩藻聚糖硫酸酯通过抑制炎症信号通路NF-κB,显著改善胰岛素抵抗模型小鼠的慢性炎症。 Objective To investigate the ameliorating of fucoidan from Thelenota ananas on chronic inflammation mice and explore possible signaling pathways.Methods The model mice were established by feeding a diet of high-fat and high-fructose.Male C57BL/6 mice were randomly divided into normal control group,model control group,rosiglitazone positive control group in 1mg·kg^-1·d^-1 dosage,Ta-FUC low group in 20mg·kg^-1·d^-1 dosage and Ta-FUC high group in 80mg·kg^-1·d^-1 dosage.All animals were fed with diet and water freely for 13 weeks.After 13 weeks treatment,the white adipose tissues were weighed,the serum glucose and insulin levels,inflammatory cytokines and inflammation signaling pathway-related genes mRNA expression were tested.Results Ta-FUC could respectively markedly decrease body fat ratio,cause a reduction of blood sugar and insulin levels,restrain insulin resistance,lower serum proinflammatory factors FFA,TNF-α,IL-6,resistin,leptin and CRP levels,increase serum anti-inflammatory factors IL-10 and Adiponectin levels,significantly inhibit inflammation signaling pathway NF-κB.Conclusion Fucoidan fromThelenota ananas inhibited inflammatory reaction in insulin resistant mice through inflammation signaling pathway NF-κB.
出处 《中国海洋药物》 CAS CSCD 2016年第2期51-58,共8页 Chinese Journal of Marine Drugs
基金 国家自然科学基金项目(31471684)资助
关键词 梅花参 岩藻聚糖硫酸酯 胰岛素抵抗 炎症 NF-ΚB Thelenota ananas fucoidan insulin resistance inflammation NF-κB
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