归肾二仙汤通过抑制PI3K/Akt/FOXO3a通路介导的氧化应激和颗粒细胞DNA断裂,改善卵巢早衰大鼠卵巢功能。

IF 2 4区 生物学 Q3 CELL BIOLOGY
Huanmei Zhong, Yuhua He, Wenhui Wang, Yingyun Liu, Danna Chen, Yongqi Shen, Chengjie Liang
{"title":"归肾二仙汤通过抑制PI3K/Akt/FOXO3a通路介导的氧化应激和颗粒细胞DNA断裂,改善卵巢早衰大鼠卵巢功能。","authors":"Huanmei Zhong, Yuhua He, Wenhui Wang, Yingyun Liu, Danna Chen, Yongqi Shen, Chengjie Liang","doi":"10.14670/HH-18-984","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>The aim of this study was to establish a rat model of premature ovarian failure (POF) with cyclophosphamide (CTX), and explore the molecular basis of POF and the mechanism of Guishen-Erxian Decoction (GSEXD) to improve POF from the perspective of oxidative stress regulation of ovarian granulosa cell (OGC) DNA fragmentation.</p><p><strong>Method: </strong>The study utilized SD rats to establish a POF model via CTX. Rats were divided into Control, POF group, three GSEXD dosage groups (low, medium, high), and a GSEXD+PI3K agonist group to assess GSEXD's therapeutic effects on oxidative stress, DNA fragmentation and ovarian damage.</p><p><strong>Result: </strong>GSEXD can improve the body weight, ovarian index, pathological status, and hormone secretion of POF rats, and inhibit ovarian oxidative stress and DNA fragmentation. In addition, GSEXD inhibits the activation of the PI3K/Akt/FoxO3a pathway. PI3K agonist 740 Y-P can reverse the effects of GSEXD on ovarian function, ovarian antioxidant capacity, and granulosa cell DNA fragmentation in POF rats.</p><p><strong>Conclusion: </strong>Inhibition of oxidative stress damage and excessive DNA fragmentation of granulosa cells is a key pathway for GSEXD to promote follicle growth and development and alleviate ovarian function decline, which may be related to the inhibition of the PI3K/AKT/FOXO3a pathway by GSEXD.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18984"},"PeriodicalIF":2.0000,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Guishen-erxian Decoction can improve ovarian function in rats with premature ovarian failure by inhibiting oxidative stress and granulosa cell DNA fragmentation mediated by the PI3K/Akt/FOXO3a pathway.\",\"authors\":\"Huanmei Zhong, Yuhua He, Wenhui Wang, Yingyun Liu, Danna Chen, Yongqi Shen, Chengjie Liang\",\"doi\":\"10.14670/HH-18-984\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>The aim of this study was to establish a rat model of premature ovarian failure (POF) with cyclophosphamide (CTX), and explore the molecular basis of POF and the mechanism of Guishen-Erxian Decoction (GSEXD) to improve POF from the perspective of oxidative stress regulation of ovarian granulosa cell (OGC) DNA fragmentation.</p><p><strong>Method: </strong>The study utilized SD rats to establish a POF model via CTX. Rats were divided into Control, POF group, three GSEXD dosage groups (low, medium, high), and a GSEXD+PI3K agonist group to assess GSEXD's therapeutic effects on oxidative stress, DNA fragmentation and ovarian damage.</p><p><strong>Result: </strong>GSEXD can improve the body weight, ovarian index, pathological status, and hormone secretion of POF rats, and inhibit ovarian oxidative stress and DNA fragmentation. In addition, GSEXD inhibits the activation of the PI3K/Akt/FoxO3a pathway. PI3K agonist 740 Y-P can reverse the effects of GSEXD on ovarian function, ovarian antioxidant capacity, and granulosa cell DNA fragmentation in POF rats.</p><p><strong>Conclusion: </strong>Inhibition of oxidative stress damage and excessive DNA fragmentation of granulosa cells is a key pathway for GSEXD to promote follicle growth and development and alleviate ovarian function decline, which may be related to the inhibition of the PI3K/AKT/FOXO3a pathway by GSEXD.</p>\",\"PeriodicalId\":13164,\"journal\":{\"name\":\"Histology and histopathology\",\"volume\":\" \",\"pages\":\"18984\"},\"PeriodicalIF\":2.0000,\"publicationDate\":\"2025-09-11\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Histology and histopathology\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.14670/HH-18-984\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Histology and histopathology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.14670/HH-18-984","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

背景:本研究旨在环磷酰胺(CTX)诱导大鼠卵巢早衰(POF)模型,并从氧化应激调节卵巢颗粒细胞(OGC) DNA断裂的角度探讨POF的分子基础及归肾二仙汤(GSEXD)改善POF的机制。方法:采用SD大鼠CTX建立POF模型。将大鼠分为对照组、POF组、GSEXD低、中、高3个剂量组和GSEXD+PI3K激动剂组,评估GSEXD对氧化应激、DNA断裂和卵巢损伤的治疗作用。结果:GSEXD能改善POF大鼠的体重、卵巢指数、病理状态和激素分泌,抑制卵巢氧化应激和DNA断裂。此外,GSEXD抑制PI3K/Akt/FoxO3a通路的激活。PI3K激动剂740 Y-P可逆转GSEXD对POF大鼠卵巢功能、卵巢抗氧化能力和颗粒细胞DNA断裂的影响。结论:抑制颗粒细胞氧化应激损伤和DNA过度断裂是GSEXD促进卵泡生长发育、缓解卵巢功能下降的关键途径,可能与GSEXD抑制PI3K/AKT/FOXO3a通路有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Guishen-erxian Decoction can improve ovarian function in rats with premature ovarian failure by inhibiting oxidative stress and granulosa cell DNA fragmentation mediated by the PI3K/Akt/FOXO3a pathway.

Background: The aim of this study was to establish a rat model of premature ovarian failure (POF) with cyclophosphamide (CTX), and explore the molecular basis of POF and the mechanism of Guishen-Erxian Decoction (GSEXD) to improve POF from the perspective of oxidative stress regulation of ovarian granulosa cell (OGC) DNA fragmentation.

Method: The study utilized SD rats to establish a POF model via CTX. Rats were divided into Control, POF group, three GSEXD dosage groups (low, medium, high), and a GSEXD+PI3K agonist group to assess GSEXD's therapeutic effects on oxidative stress, DNA fragmentation and ovarian damage.

Result: GSEXD can improve the body weight, ovarian index, pathological status, and hormone secretion of POF rats, and inhibit ovarian oxidative stress and DNA fragmentation. In addition, GSEXD inhibits the activation of the PI3K/Akt/FoxO3a pathway. PI3K agonist 740 Y-P can reverse the effects of GSEXD on ovarian function, ovarian antioxidant capacity, and granulosa cell DNA fragmentation in POF rats.

Conclusion: Inhibition of oxidative stress damage and excessive DNA fragmentation of granulosa cells is a key pathway for GSEXD to promote follicle growth and development and alleviate ovarian function decline, which may be related to the inhibition of the PI3K/AKT/FOXO3a pathway by GSEXD.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Histology and histopathology
Histology and histopathology 生物-病理学
CiteScore
3.90
自引率
0.00%
发文量
232
审稿时长
2 months
期刊介绍: HISTOLOGY AND HISTOPATHOLOGY is a peer-reviewed international journal, the purpose of which is to publish original and review articles in all fields of the microscopical morphology, cell biology and tissue engineering; high quality is the overall consideration. Its format is the standard international size of 21 x 27.7 cm. One volume is published every year (more than 1,300 pages, approximately 90 original works and 40 reviews). Each volume consists of 12 numbers published monthly online. The printed version of the journal includes 4 books every year; each of them compiles 3 numbers previously published online.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信