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目的研究海地瓜岩藻聚糖硫酸酯(fucoidan form Acaudina molpadioidea,Am-FUC)对胰岛素抵抗小鼠肝脏炎症反应的改善作用及机制。方法采用饲喂高脂高糖饲料法建立胰岛素抵抗小鼠模型,给予80mg/kg·bw的Am-FUC 19w。实验结束后,检测模型小鼠血清促炎症因子和抗炎症因子浓度和血清和肝脏FFA水平,用实时荧光定量PCR方法检测Am-FUC对肝脏组织炎症状因子基因m RNA表达,Western blotting法检测Am-FUC对胰岛素抵抗小鼠肝脏组织JNK和IKKβ/NFκB炎症通路的影响。结果 Am-FUC能显著地降低胰岛素抵抗小鼠血清促炎症因子浓度并增加抑炎症因子浓度(P<0.01),降低血清和肝脏FFA浓度(P<0.01),抑制抑炎症因子基因m RNA表达水平并促进抑炎症因子基因m RNA表达水平(P<0.05,P<0.01),抑制肝脏组织JNK1和IKKβ蛋白磷酸化(P<0.05,P<0.01)、增加细胞质中NFκB蛋白表达(P<0.01),抑制细胞核中NFκB蛋白表达(P<0.01)。结论 Am-FUC能通过抑制JNK和IKKβ/NFκB炎症通路起到改善胰岛素抵抗小鼠肝脏炎症反应的作用。
Objective To study the effect and mechanism of fucoidan form Acaudina molpadioidea (Am-FUC) on hepatic inflammatory response in insulin resistant mice. Methods The mouse model of insulin resistance was established by feeding high-fat and high-sugar diet, and Am-FUC 19w was given at 80mg / kg · bw. At the end of the experiment, serum proinflammatory cytokines and anti-inflammatory cytokines and serum and liver FFA levels were detected in mice. Real-time fluorescence quantitative PCR was used to detect the mRNA expression of hepatic tissue inflammatory factor genes by real-time fluorescence quantitative PCR. The expression of Am -FUC on JNK and IKKβ / NFκB Inflammation Pathway in Liver Tissue of Insulin-resistant Mice. Results Am-FUC could significantly decrease serum proinflammatory cytokines and increase the concentration of anti-inflammatory cytokines (P <0.01), decrease the concentration of FFA in serum and liver (P <0.01) and inhibit the mRNA expression of anti-inflammatory cytokines (P <0.05, P <0.01), and inhibited the protein phosphorylation of JNK1 and IKKβ (P <0.05, P <0.01), and increased the expression of NFκB in the cytoplasm (P <0.01) , Inhibited NFκB protein expression in the nucleus (P <0.01). Conclusion Am-FUC can improve the hepatic inflammatory response in insulin-resistant mice by inhibiting the JNK and IKKβ / NFκB inflammatory pathways.