Evidence map›Paper›PMID 40931880›Full record

ArticleHistology and histopathology2026

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.

Huanmei Zhong, Yuhua He, Wenhui Wang, Yingyun Liu, Danna Chen, Yongqi Shen, Chengjie Liang

Abstract read
PubMed Publisher
In one paragraph

Article in Histology and histopathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Huanmei Zhong *Department of Clinical Laboratory, The Fourth Affiliated Hospital of Guangzhou Medical University (Zengcheng District People's Hospital), Guangzhou, China.
Yuhua He *Department of Clinical Laboratory, The Fourth Affiliated Hospital of Guangzhou Medical University (Zengcheng District People's Hospital), Guangzhou, China.
Wenhui WangDepartment of Clinical Laboratory, The Fourth Affiliated Hospital of Guangzhou Medical University (Zengcheng District People's Hospital), Guangzhou, China.
Yingyun LiuDepartment of Clinical Laboratory, The Fourth Affiliated Hospital of Guangzhou Medical University (Zengcheng District People's Hospital), Guangzhou, China.
Danna ChenDepartment of Clinical Laboratory, The Fourth Affiliated Hospital of Guangzhou Medical University (Zengcheng District People's Hospital), Guangzhou, China.
Yongqi ShenDepartment of Clinical Laboratory, The Fourth Affiliated Hospital of Guangzhou Medical University (Zengcheng District People's Hospital), Guangzhou, China.
Chengjie LiangCenter for Experimental Teaching, School of Pharmacy, Guangzhou Medical University, Guangzhou, China. liangchengjie05@126.com.

Funding

Medical Science and Technology Foundation of Guangdong Province B2023085
6 · The paper itself

Abstract

backgroundThe 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.

methodThe 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.

resultGSEXD 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.

conclusionInhibition 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.

Indexed as

DNA FragmentationDrugs, Chinese HerbalGranulosa CellsOvaryOxidative StressPrimary Ovarian InsufficiencyAnimalsCyclophosphamideDisease Models, AnimalFemaleForkhead Box Protein O3Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleySignal TransductionCyclophosphamideDrugs, Chinese HerbalForkhead Box Protein O3FOXO3 protein, ratPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-akt

Identifiers

PMID40931880

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.