胡世伟,王静凤,徐慧,等.冰岛刺参岩藻聚糖硫酸酯对胰岛素抵抗小鼠炎症改善作用的研究[J].中国海洋药物,2015,34(6):49-56.
冰岛刺参岩藻聚糖硫酸酯对胰岛素抵抗小鼠炎症改善作用的研究
Alleviating inflammatory response of fucoidan from Cucumaria frondosa on in insulin resistant mice
投稿时间:2015-03-31  修订日期:2015-04-21
DOI:
中文关键词:  海参岩藻聚糖硫酸酯  胰岛素抵抗  炎症细胞因子  氨基端激酶  核转录因子κB
English Keywords:fucoidan from sea cucumber  insulin resistance  inflammatory cytokines  C-Jun NH2-terminal kinase  nuclear factor kappa B
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作者单位E-mail
胡世伟* 浙江海洋学院 hushiweihai@163.com 
王静凤 中国海洋大学  
徐慧 中国海洋大学  
宋文东 浙江海洋学院创新应用研究院  
夏松养 浙江海洋学院创新应用研究院  
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中文摘要:
      目的 研究冰岛刺参岩藻聚糖硫酸酯(fucoidan from the sea cucumber Cucumaria frondosa, Cf-FUC)对胰岛素抵抗小鼠炎症反应的改善作用。方法 以高脂高糖饲料饲喂法建立胰岛素抵抗小鼠模型。雄性C57BL/6J小鼠随机分为正常对照组、模型对照组、阳性对照组、Cf-FUC组。正常对照组饲喂标准饲料,其它组饲喂高脂饲料。阳性对照组、Cf-FUC组分别在饲料中添加罗格列酮(rosiglitazone, RSG, 1 mg?kg?1?d?1)、Cf-FUC (80 mg?kg?1?d?1)。各组小鼠自由摄食摄水19周。实验结束后,检测血清肿瘤坏死因子α(TNF-α)、MIP-1、IL-1β、IL-6和IL-10表达水平,荧光定量PCR方法检测小鼠脂肪组织炎症细胞因子基因mRNA表达水平,Western方法检测JNK1、IKKβ磷酸化蛋白水平及细胞核和细胞质中NFκB蛋白表达量。结果Cf-FUC可显著降低胰岛素抵抗小鼠血清TNF-α、MIP-1、IL-1β和IL-6浓度,增加IL-10浓度;抑制小鼠脂肪组织TNF-α、MIP-1、IL-1β和IL-6基因mRNA表达,促进IL-10基因mRNA表达;抑制JNK1和IKKβ的磷酸化,增加细胞质中NFκB蛋白表达量,减少细胞核中NFκB蛋白表达量。结论Cf-FUC能通过抑制JNK和IKKβ/NFκB信号通路抑制促炎症因子分泌,增加抑炎症因子分泌,改善胰岛素抵抗小鼠的炎症反应。
English Summary:
      To unravel the effects of fucoidan from the sea cucumber Cucumaria frondosa (Cf-FUC) on ameliorating inflammatory response in insulin resistant mice. Methods The insulin resistant model mice were established by feeding a diet of high-fat and high-sucrose. Male C57BL/6J mice were randomly assigned into the normal control group, the model control group, the positive control group, and Cf-FUC group. The mice in the normal control group were fed the standard diet, and the animals in the other groups were fed the high-fat diet. Rosiglitazone (RSG, 1 mg?kg?1?d?1) and Cf-FUC (80 mg?kg?1?d?1) were added into the diets of the positive control and Cf-FUC groups, respectively. All animals were fed with diet and water freely for 19 weeks. After experiments, serum tumor necrosis factor-α (TNF-α), MIP-1, IL-1β, IL-6, and IL-10 levels were determined. The mRNA expression of inflammatory cytokines genes in adipose tissues was detected using quantitative real-time PCR. The phosphorylated protein expression of JNK1 and IKKβ, as well as NFκB protein expression in cell nucleus and cytoplasm were assayed using Western blotting. Results Cf-FUC decreased serum TNF-α, MIP-1, IL-1β, and IL-6 concentrations significantly and increased IL-10 level of insulin resistant mice. Cf-FUC significantly inhibited TNF-α, MIP-1, IL-1β, and IL-6 genes mRNA expression, and promoted IL-10 gene mRNA expression in adipose tissues. Cf-FUC inhibited JNK1 and IKKβ phosphorylation, increased NFκB protein expression in cytoplasm, and reduced NFκB protein expression in cell nucleus. Conclusion Cf-FUC significantly inhibited the secretion of pro-inflammatory cytokines, increased the secretion of anti-inflammatory cytokines, and alleviated inflammatory response via inhibiting JNK and IKKβ/NFκB signal channel of insulin resistant mice.
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