Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, PR China.
Mol Cell Endocrinol. 2012 Oct 15;362(1-2):128-38. doi: 10.1016/j.mce.2012.06.002. Epub 2012 Jun 12.
The aim of the present study was to determine the effect of baicalein on metabolic syndrome induced by a high-fat diet in mice. The mice developed obesity, dyslipidemia, fatty liver, diabetes and insulin resistance. These disorders were effectively normalized in baicalein-treated mice. Further investigation revealed that the inhibitory effect on inflammation and insulin resistance was mediated by inhibition of the MAPKs pathway and activation of the IRS1/PI3K/Akt pathway. The lipid-lowering effect was attributed to the blocking of synthesis way mediated by SERBP-1c, PPARγ and the increased fatty acid oxidation. All of these effects depended on AMPKα activation. These results were confirmed in the primary hepatocytes from wild type and AMPKα(2)(-/-) mice. However, the IRS-1/PI3K/AKT pathway showed no change, which may be due to the time of stimulation and concentration. Thus, these data suggested that baicalein protects mice from metabolic syndrome through an AMPKα(2)-dependent mechanism involving multiple intracellular signaling pathways.
本研究旨在探讨黄芩素对高脂饮食诱导的小鼠代谢综合征的影响。高脂饮食诱导的小鼠出现肥胖、血脂异常、脂肪肝、糖尿病和胰岛素抵抗等代谢紊乱。黄芩素治疗可有效改善这些代谢紊乱。进一步研究发现，黄芩素通过抑制 MAPK 通路和激活 IRS1/PI3K/Akt 通路，发挥其抗炎和改善胰岛素抵抗的作用。其降脂作用与阻断 SERBP-1c、PPARγ 介导的合成途径以及增加脂肪酸氧化有关。这些作用均依赖于 AMPKα 的激活。这些结果在野生型和 AMPKα(2)(-/-)小鼠的原代肝细胞中得到了验证。然而，IRS-1/PI3K/AKT 通路没有变化，这可能与刺激时间和浓度有关。因此，这些数据表明，黄芩素通过 AMPKα(2)依赖性机制，涉及多种细胞内信号通路，保护小鼠免受代谢综合征的影响。
