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脱氢表雄酮(DHEA)可保护人颗粒HO23细胞的线粒体免受凋亡和坏死性凋亡的双重影响。

DHEA protects mitochondria against dual modes of apoptosis and necroptosis in human granulosa HO23 cells.

作者信息

Tsui Kuan-Hao, Wang Peng-Hui, Lin Li-Te, Li Chia-Jung

机构信息

Department of Obstetrics and GynecologyKaohsiung Veterans General Hospital, Kaohsiung, Taiwan

Department of Obstetrics and GynecologyNational Yang-Ming University School of Medicine, Taipei, Taiwan.

出版信息

Reproduction. 2017 Aug;154(2):101-110. doi: 10.1530/REP-17-0016.

DOI:10.1530/REP-17-0016
PMID:28624766
Abstract

Because ovarian granulosa cells are essential for oocyte maturation and development, we validated human granulosa HO23 cells to evaluate the ability of the DHEA to prevent cell death after starvation. The present study was aimed to investigate whether DHEA could protect against starvation-induced apoptosis and necroptosis in human oocyte granulosa HO23 cells. The starvation was induced by treatment of serum-free (SF) medium for 4 h Starvation-induced mitochondrial depolarization, cytochrome release and caspase-3 activation were largely prevented by DHEA in HO23 cells. We found that treatment with DHEA can restore starvation-induced reactive oxygen species (ROS) generation and mitochondrial membrane potential imbalance. In addition, treatment of DHEA prevents cell death via upregulation of cytochrome and downregulation of BAX in mitochondria. Most importantly, DHEA is ameliorated to mitochondrial function mediated through the decrease in mitochondrial ROS, maintained mitochondrial morphology, and enhancing the ability of cell proliferation and ROS scavenging. Our present data strongly indicate that DHEA reduces programmed cell death (apoptosis and necroptosis) in granulosa HO23 cells through multiple interactions with the mitochondrion-dependent programmed cell death pathway. Taken together, our data suggest that the presence of DHEA could be beneficial to protect human oocyte granulosa HO23 cells under culture conditions during various assisted reproductive technology (ART) programs.Free Chinese abstract: A Chinese translation of this abstract is freely available at http://www.reproduction-online.org/content/154/2/101/suppl/DC1.

摘要

由于卵巢颗粒细胞对卵母细胞的成熟和发育至关重要,我们验证了人颗粒HO23细胞,以评估脱氢表雄酮(DHEA)在饥饿后预防细胞死亡的能力。本研究旨在调查DHEA是否能保护人卵母细胞颗粒HO23细胞免受饥饿诱导的凋亡和坏死性凋亡。通过在无血清(SF)培养基中处理4小时来诱导饥饿。在HO23细胞中,DHEA在很大程度上预防了饥饿诱导的线粒体去极化、细胞色素释放和半胱天冬酶-3激活。我们发现,用DHEA处理可以恢复饥饿诱导的活性氧(ROS)生成和线粒体膜电位失衡。此外,DHEA处理通过上调线粒体中的细胞色素并下调BAX来预防细胞死亡。最重要的是,DHEA通过降低线粒体ROS、维持线粒体形态以及增强细胞增殖和ROS清除能力来改善线粒体功能。我们目前的数据强烈表明,DHEA通过与线粒体依赖性程序性细胞死亡途径的多种相互作用,减少颗粒HO23细胞中的程序性细胞死亡(凋亡和坏死性凋亡)。综上所述,我们的数据表明,在各种辅助生殖技术(ART)程序的培养条件下,DHEA的存在可能有利于保护人卵母细胞颗粒HO23细胞。免费中文摘要:本摘要的中文翻译可在http://www.reproduction-online.org/content/154/2/101/suppl/DC1免费获取。

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