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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,1mg·kg~(-1)·d~(-1))、Cf-FUC(80mg·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。
Objective To study the effects of fucoidan from the sea Cucumber Cucumaria frondosa (Cf-FUC) on the inflammatory response in insulin resistant mice. Methods The model of insulin resistance was established by feeding with high fat and sugar diet. Male C57BL / 6J mice were randomly divided into normal control group, model control group, positive control group and Cf-FUC group. Normal control group fed standard feed, other groups fed high-fat feed. The positive control group and the Cf-FUC group were given rosiglitazone (RSG, 1 mg · kg -1 · d -1), Cf-FUC (80 mg · kg -1 ) · D -1). The mice in each group were allowed to take water for 19 weeks. At the end of the experiment, the expression of TNF-α, MIP-1, IL-1β, IL-6 and IL-10 in serum was detected and the mRNA expression of inflammatory cytokines in adipose tissue was detected by real- Western blot was used to detect the phosphorylation of JNK1 and IKKβ and the expression of NFκB in nucleus and cytoplasm. Results Cf-FUC could significantly decrease the concentration of TNF-α, MIP-1, IL-1β and IL-6 in serum and increase the concentration of IL-10 in mice with insulin resistance. 1β and IL-6 mRNA and IL-10 mRNA, and inhibited the phosphorylation of JNK1 and IKKβ, increased the expression of NFκB in the cytoplasm and decreased the expression of NFκB in the nucleus. Conclusion Cf-FUC can inhibit the secretion of proinflammatory cytokines by inhibiting JNK and IKKβ / NFκB signaling pathways, increase the secretion of anti-inflammatory cytokines and improve the inflammatory response in insulin-resistant mice.