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Aging Cell：二甲双胍延缓人类细胞衰老的新机制

2018-04-23 佚名 中科院生物物理所

二甲双胍GPx7衰老
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近日，Aging cell杂志发表了中国科学院生物物理研究所王志珍课题组与刘光慧课题组合作完成的研究论文Metformin alleviates human cellular aging by upregulating theendoplasmic reticulum glutathione peroxidase 7。该研究发现低剂量二甲双胍可通过上调内质网谷胱甘肽过氧化物酶7（GPx7）的表达延

近日，Aging cell杂志发表了中国科学院生物物理研究所王志珍课题组与刘光慧课题组合作完成的研究论文Metformin alleviates human cellular aging by upregulating theendoplasmic reticulum glutathione peroxidase 7。该研究发现低剂量二甲双胍可通过上调内质网谷胱甘肽过氧化物酶7（GPx7）的表达延缓正常人类细胞的衰老进程，为干预人类衰老提供了新的潜在靶点和新思路。

二甲双胍是目前治疗2型糖尿病的一线药物。近年来，陆续有研究报道二甲双胍具有延缓低等动物衰老的能力。然而，人们尚不清楚二甲双胍是否对人类的细胞衰老也具有保护作用。

研究发现，长时间、低剂量（与服用二甲双胍的糖尿病患者静脉血中的药物浓度相近）的二甲双胍处理，可延缓人类二倍体成纤维细胞和间充质干细胞的复制性衰老。同时发现，二甲双胍可增强抗氧化转录因子Nrf2的转录活性进而上调内质网GPx7的表达。王志珍课题组的前期研究表明GPx7在内质网蛋白质的氧化折叠和氧化还原稳态维持中起到重要作用（Antioxid Redox Signal， 2014）。该研究发现GPx7的表达水平随着人类细胞衰老显着降低，而敲低GPx7可加速人类细胞衰老并促进体内干细胞的耗竭。在刘光慧课题组前期建立的Nrf2遗传增强的“长寿”干细胞中（Cell Research， 2017），GPx7的表达水平明显升高。有趣的是，Nrf2-GPx7信号通路在二甲双胍诱导的线虫寿命延长中亦起着关键性作用。二甲双胍可通过激活线虫中Nrf2的同源蛋白进而上调线虫GPX-6（人源GPx7的同源物）的表达；而敲低GPX-6可显着抑制二甲双胍对线虫的延寿作用。

该项研究为二甲双胍延缓人类细胞衰老提供了重要的实验证据和机制探索，并建立了内质网氧化还原状态与人类细胞衰老之间的科学联系。同时，靶向Nrf2-GPx7通路也为衰老相关疾病的预防和治疗提供新的思路。

该研究受到国家重点研发计划、国家自然科学基金、中科院战略先导专项以及中科院青年创新促进会等项目的资助。

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    2018-11-07 zhaozhouchifen

    #Cell#

    0

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    2018-08-01 维他命

    #CEL#

    0

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    2018-04-25 ms8543593053280928

    #细胞衰老#

    0

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    2018-04-24 kafei

    学习学习

    0

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    2018-04-23 871538379

    很多降糖药都对改善脑代谢及认知有推动作用

    0

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    2018-04-23 医者仁心5538

    学习了

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    2018-04-23 sunfeifeiyang

    阅

    0

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