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gonadotrophin-releasing hormone-Ⅰ and -Ⅱ stimulate steroidogenesis in prepubertal murine Leydig cells in vitro

Asian Journal of Andrology 2008年第6期10卷 929-936页

作者： Yung-Ming Lin Ming-Yie Liu Song-Ling Poon Sew-Fen Leu Bu-Miin Huang Department of Urology College of Medicine National Cheng Kung University Tainan 70101 Taiwan China Department of Environmental and Occupational Health College of Medicine National Cheng Kung University Tainan 70101 Taiwan China Department of Cell Biology and Anatomy College of Medicine National Cheng Kung University Tainan 70101 Taiwan China Institute of Bioindustrial Technology College of Human Ecology HungKuang University Taichung 43302 Taiwan China

Aim： To study the effect and mechanism of gonadotrophin-releasing hormone （GnRH） on murine Leydig cell steroidogenesis. Methods： Purified murine Leydig cells were treated with GnRH-Ⅰ and -Ⅱ agonists, and testosterone production and steroidogenic enzyme expressions were determined. Results： GnRH-Ⅰ and -Ⅱ agonists significantly stimulated murine Leydig cell steroidogenesis 60%-80% in a dose- and time-dependent manner （P 〈 0.05）. The mRNA expressions of steroidogenic acute regulatory （STAR） protein, P450scc, 3β-hydroxysteroid dehydrogenase （HSD）, but not 17β-hydroxylase or 17β-HSD, were significantly stimulated by both GnRH agonists with a 1.5- to 3-fold increase （P 〈 0.05）. However, only 3β-HSD protein expression was induced by both GnRH agonists, with a 1.6- to 2-fold increase （P 〈 0.05）. Conclusion： GnRH directly stimulated murine Leydig cell steroidogenesis by activating 3β-HSD enzyme expression.

关键词： gonadotrophin-releasing hormone Leydig cells murine steroidogenesis stimulation

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Influence of gonadotropin-releasing hormone agonist on the effect of chemotherapy upon ovarian cancer and the prevention of chemotherapy-induced ovarian damage:an experimental study with nu/nu athymic mice

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2012年第11期13卷 894-903页

作者： Qiong-yan LIN Yi-feng WANG Hui-nan WENG Xiu-jie SHENG Qing-ping JIANG Zhi-ying YANG Department of Obstetrics and Gynecology Key Laboratory for Major Obstetric Diseases of Guangdong Province the Third Affiliated Hospital of Guangzhou Medical University Guangzhou 510150 China Department of Obstetrics and Gynecology Zhujiang Hospital Nanfang Medical University Guangzhou 510282 China

Background and objective:Gonadotropin-releasing hormone (GnRH) plays an important role in the regulation of ovarian function and ovarian cancer cell growth. In this study, we determined whether administration of the GnRH agonist (GnRHa), triporelin, prior to cisplatin treatment affects cisplatin and/or prevents cisplatin-induced ovarian damage. Methods:nu/nu mice were injected with ovarian cancer OVCAR-3 cells intraperitoneally. After two weeks, the mice were treated with saline (control), cisplatin, GnRHa, or cisplatin plus GnRHa for four weeks. At the end of the experimental protocol, blood, tumor, ovary, and uterine tissues were resected for hematoxylin and eosin (H&E) staining, immunohistochemical analyses of Ki67, nuclear factor-κB (NF-κB), and caspase-3, transmission electron microscopy of apoptosis, or enzyme-linked immunosorbent assay (ELISA) analyses of anti-Mullerian hormone (AMH). Results:Cisplatin treatment effectively inhibited tumor growth in mice treated with human ovarian cancer cells; however the treatment also induced considerable toxicity. Immunohistochemical analyses showed that Ki67 expression was reduced in cisplatin-treated mice compared to control (P0.05), while expressions of NF-κB and caspase-3 were reduced and induced, respectively, in cisplatin-treated mice and cisplatin plus GnRHa-treated mice. Apoptosis occurred in the GnRHa, cisplatin, and cisplatin plus GnRHa-treated mice, but not in control mice. Ovaries exposed to GnRHa in both GnRHa mice and cisplatin-treated mice (combination group) had significantly more primordial and growth follicles and serum levels of AMH than those in the control mice and cisplatin-treated mice (P<0.05). Conclusions:Administration of GnRHa to mice significantly decreased the extent of ovarian damage induced by cisplatin, but did not affect the anti-tumor activity of cisplatin

关键词： gonadotrophin-releasing hormone Cisplatin Ovarian cancer Animal experiment

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