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候丽琼, 赵铁耘, 张伊祎. 黄连素对肥胖胰岛素抵抗大鼠骨骼肌胰岛素抵抗的干预研究[J]. 四川大学学报(医学版), 2015, 46(6): 827-831.
引用本文: 候丽琼, 赵铁耘, 张伊祎. 黄连素对肥胖胰岛素抵抗大鼠骨骼肌胰岛素抵抗的干预研究[J]. 四川大学学报(医学版), 2015, 46(6): 827-831.
HOU Li-qiong, ZHAO Tie-yun, ZHANG Yi-yi. Effect of Berberine on the Insulin Resistance and TLR4/IKKβ/NF-κB Signaling Pathways in Skeletal Muscle of Obese Rats with Insulin Resistance[J]. Journal of Sichuan University (Medical Sciences), 2015, 46(6): 827-831.
Citation: HOU Li-qiong, ZHAO Tie-yun, ZHANG Yi-yi. Effect of Berberine on the Insulin Resistance and TLR4/IKKβ/NF-κB Signaling Pathways in Skeletal Muscle of Obese Rats with Insulin Resistance[J]. Journal of Sichuan University (Medical Sciences), 2015, 46(6): 827-831.

黄连素对肥胖胰岛素抵抗大鼠骨骼肌胰岛素抵抗的干预研究

Effect of Berberine on the Insulin Resistance and TLR4/IKKβ/NF-κB Signaling Pathways in Skeletal Muscle of Obese Rats with Insulin Resistance

  • 摘要: 目的 探讨黄连素改善肥胖胰岛素抵抗大鼠骨骼肌胰岛素抵抗的可能机制。 方法 40只Wistar大鼠分为高脂组(HF组,30只)和正常对照组(NC组,10只)。成模后处理NC组10只及HF组10只大鼠。检测血浆中内毒素(ET)水平,RT-PCR检测骨骼肌中 Toll样受体4(TLR4) mRNA ,Western blot检测骨骼肌TLR4、IκB激酶(IKKβ)、IKKβ 181位丝氨酸磷酸化(p-IKKβSer181、核因子κB(NF-κB) 、肿瘤坏死因子-α(TNF-α)蛋白表达,胰岛素受体(IR)与胰岛素受体底物(IRS)-1总蛋白及磷酸化水平。余20只肥胖大鼠分为黄连素干预组( FB组,10只)及肥胖模型对照组( FC组,10只),继续高脂饮食喂养,FB 组予200 mg/(kg·d)每日1次黄连素灌胃,FC 组予等量蒸馏水灌胃,持续8周后检测以上指标。 结果 肥胖大鼠血浆中ET水平升高,且骨骼肌TLR4/IKKβ/NF-κB内毒素信号通路激活,炎症因子TNF-α蛋白表达增加,黄连素干预使肥胖胰岛素抵抗大鼠血浆中ET水平降低,且骨骼肌组织TLR4/IKKβ/NF-κB内毒素信号通路各蛋白及TNF-α蛋白表达均下调, IR及IRS-1酪氨酸磷酸化水平均升高( P<0.05)。结论 黄连素可改善肥胖胰岛素抵抗大鼠骨骼肌胰岛素抵抗,其机制可能是通过下调骨骼肌 TLR4/IKKβ/NF-κB内毒素信号通路减少炎症因子TNF-α产生所致。

     

    Abstract: Objective To investigate the role of phosphatidylinositol 3 kinase/protein kinase B (PI3K/Akt) signaling pathway for umbilical cord-derived mesenchymal stem cells (UC-MSCs) treating in neonatal rats with hypoxia-ischemia brain damage (HIBD). Methods P10 SD rats were divided into sham group, MSCs group, inhibitor (LY 294002) group (LY group) and HIBD group randomly. To establish a neonatal rat model of HIBD, UC-MSCs labeled with Brd U were transplanted into the lateral ventricle of rats. At 24 and 48 h after transplantation, the number of apoptotic cells was detected by TUNEL, while the expression of caspase3 protein and phosphorylation of Akt (P-Akt) were quantified by Western blot. Results At 24 and 48 h after transplantation, both the apoptotic cells and caspase3 protein expression in MSCs group were less than those in LY group and HIBD group ( P<0.05), while the expression of P-Akt was higher than those in LY group and HIBD group ( P<0.05), and with the passage of time after transplantation, the expression of each index showed a downward trend. Conclusion The apoptotic cells of brain and the expression of caspase3 protein decrease, while the expression of P-Akt increase. PI3K/Akt signaling pathway may be an important mechanism for UC-MSCs transplantation in HIBD rats.

     

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