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补肾强身片对多囊卵巢综合征模型大鼠的干预作用及机制研究
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| 篇名： | 补肾强身片对多囊卵巢综合征模型大鼠的干预作用及机制研究 |
| TITLE： | Study on intervention effect of Bushen qiangshen tablet on polycystic ovary syndrome model rats and its mechanism |
| 摘要： | 目的 研究补肾强身片对多囊卵巢综合征（PCOS）模型大鼠的干预作用及机制。方法将50只大鼠灌胃来曲唑混悬液（1mg/kg，每天1次，连续21d）复制PCOS模型。将造模成功的大鼠分为模型组、阳性对照组（炔雌醇环丙孕酮片0.2mg/kg+盐酸二甲双胍片230mg/kg）和补肾强身片低、中、高剂量组（189、378、756mg/kg），每组10只。另取10只未造模大鼠作为正常组。各组大鼠给予相应药物干预，每天1次，连续30d。末次给药24h后，检测大鼠血清中雌二醇（E2）、睾酮（T）、促性腺激素释放激素（GnRH）、促卵泡激素（FSH）和促黄体生成素（LH）水平，计算大鼠卵巢系数，观察大鼠卵巢组织病理形态学变化，检测大鼠卵巢组织中磷脂酰肌醇3激酶（PI3K）、磷酸化蛋白激酶B（p-Akt）、磷酸化哺乳动物雷帕霉素靶蛋白（p-mTOR）和葡萄糖转运蛋白4（GLUT4）的表达水平以及PI3K、Akt、mTOR、GLUT4mRNA表达水平。结果与正常组比较，模型组大鼠卵巢系数、卵巢囊性病变评分均显著增加（P＜0.05），血清中T、GnRH、LH水平均显著升高（P＜0.05），血清中FSH、E2水平和卵巢组织中PI3K、p-Akt、p-mTOR、GLUT4蛋白表达水平及PI3K、Akt、mTOR、GLUT4mRNA表达水平均显著降低（P＜0.05），卵巢组织中闭锁卵泡及无卵丘的囊性卵泡数量增多，卵泡颗粒细胞层数减少。与模型组比较，补肾强身片中、高剂量组大鼠上述指标水平均显著逆转（P＜0.05），低剂量组上述大部分指标水平显著逆转（P＜0.05），卵巢组织病变均不同程度改善。结论补肾强身片可调节PCOS模型大鼠性激素分泌水平，改善卵巢囊性病变，其作用机制可能与上调PI3K/Akt/mTOR、PI3K/Akt/GLUT4两条信号通路有关。 |
| ABSTRACT： | OBJECTIVE To study the intervention effect of Bushen qiangshen tablet on polycystic ovary syndrome （PCOS） model rats and its mechanism . METHODS Totally 50 rats were given letrozole suspension （1 mg/kg，once a day ，for consecutive 21 d） instragastrically to induce PCOS model . Model rars were randomly divided into model group ，positive control group （Ethinylestradiol and cyproterone acetate tables 0.2 mg/kg+Metformin hydrochloride tables 230 mg/kg），Bushen qiangshen tablet low-dose，medium-dose and high -dose groups （189，378，756 mg/kg），with 10 rats in each group . Another 10 healthy rats were included in normal group . Each group was given the corresponding drugs ，once a day ，for consecutive 30 d. Twenty-four hours after the last administration ，serum levels of estrogen （E2），testosterone（T），gonadotropin-releasing hormone （GnRH），follicle- stimulating hormone （FSH）and luteinizing hormone （LH）were measured . The ovary index was calculated ，and pathological changes of ovary were observed . The protein expressions of phosphoinositide 3-kinase（PI3K），phosphorylated protein kinase B （p- Akt），phosphorylated mammalian target of rapamycin （p-mTOR）and glucose transporter 4（GLUT4）in ovary were detected ，and mRNA expressions of PI 3K，Akt，mTOR and GLUT 4 in ovary were detected . RESULTS Compared with normal group ，ovarian index and ovarian cystic disease score were significantly increased in model group （P＜0.05），and serum levels of T ，GnRH and LH were significantly increased （P＜0.05）；serum levels of FSH and E 2，protein expressions of PI 3K，p-Akt，p-mTOR and GLUT4，and mRNA expression of PI 3K，AKT，mTOR and GLUT 4 in ovarian tissue were all significantly decreased in the model group （P＜0.05）；in ovarian tissue ，the number of atresia follicles and non -cumulus cystic follicles increased ，and the number of granulosa cell layers decreased . Compared with model group ， above indexes of Bushen qiangshen tablet medium-dose and high -dose g roups were reversed significantly 86550201。E-mail：mary868@163.com （P＜0.05），and most above indexes of low -dose group were reversed significantly （P＜0.05），the pathological changes of ovarian tissue were improved to varying degrees . CONCLUSIONS Bushen qiangshen tablet can regulate the secretion of sex hormones in PCOS model rats and improve ovarian cystic lesions . Its mechanism may be related to the upregulation of PI 3K/Akt/mTOR and PI 3K/Akt/GLUT4 signaling pathways . |
| 期刊： | 2022年第33卷第21期 |
| 作者： | 张明昊，高一盈，董文霞，薛鹏坤，马伟洋，张大伟，马丽亚 |
| AUTHORS： | ZHANG Minghao，GAO Yiying，DONG Wenxia，XUE Pengkun，MA Weiyang，ZHANG Dawei，MA Liya |
| 关键字： | 补肾强身片；多囊卵巢综合征；PI3K/Akt/mTOR信号通路；PI3K/Akt/GLUT4信号通路 |
| KEYWORDS： | Bushen qiangshen tablet ；polycystic ovary syndrome ；PI3K/Akt/mTOR signaling pathway ；PI3K/Akt/GLUT4 |
| 阅读数： | 126 次 |
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