Publication: 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
Yuhua He ; Wenhui Wang ; Yingyun Liu ; Danna Chen ; Yongqi Shen ; Chengjie Liang ; Huanmei Zhong
item.page.secondaryauthor
item.page.director
Publisher
publication.page.editor
Universidad de Murcia, Departamento de Biología Celular e Histología
publication.page.department
DOI
https://doi.org/10.14670/HH-18-984
item.page.type
info:eu-repo/semantics/article
Description
Abstract
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.
publication.page.subject
Citation
item.page.embargo
Ir a Estadísticas
Este ítem está sujeto a una licencia Creative Commons. http://creativecommons.org/licenses/by-nc/4.0/