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首页> 外文期刊>The British Journal of Nutrition >Curcumin induces mitochondrial biogenesis by increasing cyclic AMP levels via phosphodiesterase 4A inhibition in skeletal muscle
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Curcumin induces mitochondrial biogenesis by increasing cyclic AMP levels via phosphodiesterase 4A inhibition in skeletal muscle

机译：姜黄素通过抑制骨骼肌中的磷酸二酯酶 4A 增加环 AMP 水平来诱导线粒体生物发生

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Abstract Background: Previous research has suggested that curcumin potentially induces mitochondrial biogenesis in skeletal muscle via increasing cyclic AMP (cAMP) levels. However, the regulatory mechanisms for this phenomenon remain unknown. The purpose of the present study was to clarify the mechanism by which curcumin activates cAMP-related signalling pathways that upregulate mitochondrial biogenesis and respiration in skeletal muscle.Methods: The effect of curcumin treatment (i.p., 100 mg/kg-BW/d for 28 d) on mitochondrial biogenesis was determined in rats. The effects of curcumin and exercise (swimming for 2 h/d for 3 d) on the cAMP signalling pathway were determined in the absence and presence of phosphodiesterase (PDE) or protein kinase A (PKA) inhibitors. Mitochondrial respiration, citrate synthase (CS) activity, cAMP content and protein expression of cAMP/PKA signalling molecules were analysed.Results: Curcumin administration increased cytochrome c oxidase subunit (COX-IV) protein expression, and CS and complex I activity, consistent with the induction of mitochondrial biogenesis by curcumin. Mitochondrial respiration was not altered by curcumin treatment. Curcumin and PDE inhibition tended to increase cAMP levels with or without exercise. In addition, exercise increased the phosphorylation of phosphodiesterase 4A (PDE4A), whereas curcumin treatment strongly inhibited PDE4A phosphorylation regardless of exercise. Furthermore, curcumin promoted AMP-activated protein kinase (AMPK) phosphorylation and PPAR gamma coactivator (PGC-1α) deacetylation. Inhibition of PKA abolished the phosphorylation of AMPK.Conclusion: The present results suggest that curcumin increases cAMP levels via inhibition of PDE4A phosphorylation, which induces mitochondrial biogenesis through a cAMP/PKA/AMPK signalling pathway. Our data also suggest the possibility that curcumin utilises a regulatory mechanism for mitochondrial biogenesis that is distinct from the exercise-induced mechanism in skeletal muscle.
机译：摘要 背景： 先前的研究表明，姜黄素可能通过增加环腺苷酸（cAMP）水平来诱导骨骼肌中的线粒体生物发生。然而，这种现象的调节机制仍然未知。本研究的目的是阐明姜黄素激活 cAMP 相关信号通路的机制，这些通路上调骨骼肌中的线粒体生物发生和呼吸。方法：测定姜黄素处理（腹腔注射，100 mg/kg-BW/d，持续28 d）对大鼠线粒体生物发生的影响。在没有和存在磷酸二酯酶 （PDE） 或蛋白激酶 A （PKA） 抑制剂的情况下，确定姜黄素和运动（游泳 2 h/d 持续 3 d）对 cAMP 信号通路的影响。分析线粒体呼吸、柠檬酸合酶（CS）活性、cAMP含量和cAMP/PKA信号分子蛋白表达。结果：姜黄素给药增加了细胞色素c氧化酶亚基（COX-IV）蛋白的表达，以及CS和复合物I的活性，这与姜黄素诱导线粒体生物发生一致。姜黄素处理不会改变线粒体呼吸。姜黄素和PDE抑制往往会增加cAMP水平，无论是否运动。此外，运动增加了磷酸二酯酶4A（PDE4A）的磷酸化，而姜黄素治疗强烈抑制了PDE4A的磷酸化，无论运动如何。此外，姜黄素促进AMP活化蛋白激酶（AMPK）磷酸化和PPARγ共激活因子（PGC-1α）脱乙酰化。PKA的抑制消除了AMPK的磷酸化。结论：姜黄素通过抑制PDE4A磷酸化提高cAMP水平，PDE4A磷酸化通过cAMP/PKA/AMPK信号通路诱导线粒体生物发生。我们的数据还表明，姜黄素有可能利用线粒体生物发生的调节机制，这与骨骼肌中运动诱导的机制不同。

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