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Effects of nitric oxide on steroidogenesis and apoptosis in goat luteinized granulosa cells

机译：一氧化氮对山羊丁氏籽粒细胞胚胎产生和细胞凋亡的影响

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摘要

The aim of this study was to investigate effects of nitric oxide (NO) on steroidogenesis and apoptosis in goat luteinized granulosa cells (LGCs). We cultured goat LGCs from healthy follicles in culture medium supplemented with the NO donor sodium nitroprusside (SNP) or the NO synthase inhibitor N-omega-Nitro-Larginine methyl ester hydrochloride (L-NAME), then examined steroid synthesis, oxidative stress and apoptosis in vitro. The results showed that SNP treatment significantly increased the cGMP concentration in the LGCs (P & 0.05), whereas the L-NAME treatment significantly decreased cGMP concentration (P & 0.05). Then Inhibition of NO production significantly inhibited the expression of CYP19A1, a key gene that is involved in sex steroid hormones synthesis and is responsible for the decrease of E-2. Inhibition of NO production resulted in an increased percentage of apoptosis, which was accompanied by upregulating expression levels of apoptosis-related markers BAX, CASP3 and CASP9. These data indicate that NO is required for goat LGCs steroidogenesis and cell survival. Furthermore, Inhibition of NO production decreased the expression of mitochondrial biogenesis related genes and proteins (PPARGCIA, NRF-1 and TFAM) and the mtDNA copy number. Simultaneously, inhibition of NO production suppressed the transcription and translation of SOD, GPX1, and CAT, and decreased the glutathione level and increased the 8-OHdG level. However, SNP treatment increased the expression of genes involved in mitochondrial function and biogenesis, and elevated the anti-oxidant stress system and steroid synthesis. Together, our results indicate that NO may up-regulate the expression of PPARGCIA and its downstream factors through the cGMP pathway, thereby decreasing granulosa cell apoptosis, and may participate in the regulation of granulocyte steroid production through the mitochondrial-dependent pathway. (C) 2018 Elsevier Inc. All rights reserved.
机译：本研究的目的是调查一氧化氮（NO）对山羊丁氏粒化粒细胞（LGC）凋亡和细胞凋亡的影响。我们将山羊LGC从培养培养基中的健康卵泡培养，含有NOOR硝普钠（SNP）或NO合酶抑制剂N-OMEGA-NITRON-盐酸盐（L-NAME），然后检查了类固醇合成，氧化应激和凋亡体外。结果表明，SNP治疗显着增加了LGCs中的CGMP浓度（P＆amp; 0.05），而L-NAME治疗显着降低CGMP浓度（P＆amp; <0.05）。然后抑制不显着抑制CYP19A1的表达，这是涉及性类固醇激素合成的关键基因，并且负责E-2的降低。抑制不产生的产生增加的凋亡百分比增加，其伴随着上调凋亡相关标记的表达水平，Casp3和Casp9。这些数据表明山羊LGCS甾体系和细胞存活是不需要的。此外，抑制不产生的产生降低了线粒体生物发生相关基因和蛋白质（PPARGCIA，NRF-1和TFAM）和MTDNA拷贝数的表达。同时，抑制不抑制SOD，GPX1和猫的转录和翻译，并降低谷胱甘肽水平并增加8-OHDG水平。然而，SNP治疗增加了参与线粒体功能和生物发生的基因的表达，并升高了抗氧化应力系统和类固醇合成。我们的结果表明，不可能通过CGMP途径上调PPargcia及其下游因素的表达，从而降低颗粒细胞凋亡，并且可以通过线粒体依赖性途径参与调节粒细胞类固醇产生。 （c）2018年Elsevier Inc.保留所有权利。

著录项

  • 来源
    《Theriogenology》 |2019年第2019期|共8页
  • 作者

    Guo Yi-Xuan; Zhang Guo-Min; Yao Xiao-Lei; Tong Ran; Cheng Chun-Yu; Zhang Ting-Ting; Wang Shu-Ting; Yang Hua; Wang Feng;

  • 作者单位

    Nanjing Agr Univ Jiangsu Livestock Embryo Engn Lab Nanjing 210095 Jiangsu Peoples R China;

    Nanjing Agr Univ Jiangsu Livestock Embryo Engn Lab Nanjing 210095 Jiangsu Peoples R China;

    Nanjing Agr Univ Jiangsu Livestock Embryo Engn Lab Nanjing 210095 Jiangsu Peoples R China;

    Nanjing Agr Univ Jiangsu Livestock Embryo Engn Lab Nanjing 210095 Jiangsu Peoples R China;

    Nanjing Agr Univ Jiangsu Livestock Embryo Engn Lab Nanjing 210095 Jiangsu Peoples R China;

    Nanjing Agr Univ Jiangsu Livestock Embryo Engn Lab Nanjing 210095 Jiangsu Peoples R China;

    Nanjing Agr Univ Jiangsu Livestock Embryo Engn Lab Nanjing 210095 Jiangsu Peoples R China;

    Nanjing Agr Univ Jiangsu Livestock Embryo Engn Lab Nanjing 210095 Jiangsu Peoples R China;

    Nanjing Agr Univ Jiangsu Livestock Embryo Engn Lab Nanjing 210095 Jiangsu Peoples R China;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 动物学;
  • 关键词

    Goat luteinized granulosa cells; Nitric oxide; Mitochondria; Steroidogenesis; Apoptosis;

    机译：山羊丁氏鳞状颗粒细胞;一氧化氮;线粒体;甾体系;细胞凋亡;

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