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目的采用胰岛素抵抗模型小鼠研究海地瓜岩藻聚糖硫酸酯(fucoidan from Acaudina molpadioidea,Am-FUC)对慢性低度炎症反应的影响。方法以高脂高果糖饲料饲喂法建立胰岛素抵抗小鼠模型,灌胃AmFUC(80mg·kg~(-1)·d~(-1))90d。实验结束后,检测小鼠空腹血糖、空腹胰岛素水平和血清中肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、C-反应蛋白(C-reactive protein,CRP)、白细胞介素-6(interleukin-6,IL-6)、瘦素(leptin,Lep)、抵抗素(resistin,Res)、游离脂肪酸(free fatty acids,FFA)等促炎因子水平及脂联素(adiponectin,ADP)、白细胞介素~(-1)0(interleukin~(-1)0,IL~(-1)0)等抗炎因子水平;采用q-RT-PCR法检测小鼠肝脏中TNF-α、IL-6、Lep、ADP mRNA表达及NF-κB通路中关键基因IKKβ、IκB-α、NF-κB1mRNA表达。结果 AmFUC可显著降低胰岛素抵抗小鼠空腹血糖和空腹胰岛素水平;显著降低血清中促炎因子分泌及TNF-α、IL-6、Lep mRNA表达,提高抗炎因子分泌及ADP mRNA表达;显著下调NF-κB通路中关键基因NF-κB1、IKKβmRNA表达,上调IκB-αmRNA表达。结论 Am-FUC具有抑制慢性低度炎症反应作用,其作用机制与下调NF-κB信号转导通路有关。
Objective To study the effect of fucoidan from Acaudina molpadioidea (Am-FUC) on chronic low-grade inflammatory reaction in insulin resistance model mice. Methods The mice model of insulin resistance was established by feeding with high fat and high fructose diet and the mice were administered orally with AmFUC (80mg · kg -1 · d -1) for 90 days. After the experiment, the levels of fasting blood glucose, fasting insulin and levels of tumor necrosis factor-α (TNF-α), C-reactive protein (CRP) and interleukin- 6, interleukin-6, leptin, resistin, free fatty acids (FFA) and other pro-inflammatory cytokines and adiponectin (ADP) , Interleukin -1 (-1) 0 and IL -1 (-1)). The levels of TNF-α and IL-6 in the liver were detected by q-RT- -6, Lep, ADP mRNA expression and the expression of IKKβ, IκB-α, NF-κB1mRNA in NF-κB pathway. Results AmFUC significantly decreased fasting blood glucose and fasting insulin levels in insulin resistant mice, significantly decreased serum proinflammatory cytokine secretion, TNF-α, IL-6 and Lep mRNA expression, increased anti-inflammatory cytokine secretion and ADP mRNA expression, significantly decreased NF -κB pathway in key genes NF-κB1, IKKβmRNA expression, up-regulated IκB-αmRNA expression. Conclusions Am-FUC can inhibit chronic low-grade inflammatory reaction and its mechanism is related to the down-regulation of NF-κB signal transduction pathway.