| 摘要: |
| 目的应用脱氢表雄酮（DHEA）诱导多囊卵巢综合征（PCOS）大鼠模型，观察沉默信息调节因子1（SIRT1）、叉头蛋白盒转录因子3a（FoxO3a）在PCOS大鼠卵巢中的表达，探讨PCOS发病的可能机制。方法选取21日龄雌性SD大鼠20只，随机分为PCOS模型组（DHEA组）和正常对照组（NC组），DHEA组给予DHEA皮下注射，NC组给予等量芝麻油注射，两组持续给药20d。观察卵巢光镜下(HE染色)形态学改变；应用ELISA法测定血清雄激素（T）、黄体生成素（LH）、卵泡刺激素（FSH）、空腹胰岛素（FINS）、空腹血糖（FPG）、HDL、LDL、TC和TG水平；应用免疫组化法检测实验大鼠卵巢中SIRT1、FoxO3a的表达；应用荧光定时定量聚合酶链反应(real-timePCR)检测SIRT1、FoxO3amRNA的表达。结果与NC组相比，DHEA组卵巢体积明显增大。镜下见多个囊性扩张的卵泡，多见闭锁卵泡，卵泡膜细胞细胞层局部凹凸不平，颗粒细胞层几乎消失不见。血清T、LDL、TG水平明显增加（均P＜0.05）；DHEA组大鼠卵巢中SIRT1蛋白水平显著高于NC组（P＜0.01），FoxO3a水平呈升高趋势，但差异无统计学意义（P＞0.05）。DHEA组大鼠卵巢中SIRT1、FoxO3amRNA水平显著高于NC组（均P＜0.05）。结论SIRT1/FoxO3a信号通路在PCOS模型大鼠的病理过程中可能通过作用于局部卵泡微环境，调节颗粒细胞发挥作用。 |
| 关键词: 多囊卵巢综合征 沉默信息调节因子 1 叉头转录因子类 脱氢表雄酮 大鼠 |
| DOI：10.12056/j.issn.1006-2785.2018.40.5.2018-151 |
| 分类号: |
| 基金项目:浙江省科技厅重大科技专项重点社会发展项目（2014C03044-1）；杭州市科技局重点专病专科项目（20160533B35） |
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| Expression of SIRT1 and FoxO3a in ovarian tissue of rats with DHEA-induced polycystic ovarian syndrome |
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Hangzhou Hospital of Nanjing Medical University
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| Abstract: |
| Objective To investigate the expression of SIRT1 and FoxO3a in the ovarian tissue of rats with
dehydroepiandrosterone(DHEA)-induced polycystic ovarian syndrome(PCOS). Methods Twenty female SD rats were randomly divided into normal control group and PCOS group. PCOS was induced by subcutaneous injection of DHEA for 20d, while the same volume of sesame oil was injected in normal control group. Light microscopic examinations were performed. Serum T, LH, FSH, FINS, FPG, HDL, LDL, TC and TG levels in rats were determined with ELISA method. The expressions of SIRT1 and FoxO3a mRNA and proteins in ovarian tissue were detected with RT-PCR and immunohistochemistry, respectively. Results The PCOS rats exhibited increased volume of ovaries. Microscopic examination showed a number of cysts formed from atretic follicle, and a
diminished granulosa layer in rat ovaries of PCOS group. Serum levels of T, LDL and TG increased in the PCOS group, in contrast with the control group (P＜0.05). The level of SIRT1 protein in ovaries of PCOS group was significantly higher than that in control group(P＜0.05). The level of FoxO3a protein had an increasing trend in the ovaries of PCOS group but no significant difference to that of control group (P ＞0.05). The expression of both SIRT1 and FoxO3a mRNA in the ovarian tissues of PCOS group increased
significantly compared to the control group(P＜0.05). Conclusion The study indicates that SIRT1/FoxO3a signaling pathway may play a role in the pathogenesis of PCOS by regulating the granulosa in ovary. |
| Key words: Polycystic ovarian syndrome SIRT1 Forkhead transcription factors Dehydroepiandrosterone Rats |
