Evidence map›Paper›PMID 32227125›Full record

ArticleBioscience reports2020

Catalpol protects rat ovarian granulosa cells against oxidative stress and apoptosis through modulating the PI3K/Akt/mTOR signaling pathway.

Jin Yan, Disi Deng, Yeke Wu, Keming Wu, Jie Qu, Fei Li

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
7.2field-weighted citation impact, top 2% of its field
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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

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  13. The protective effects ofFrontiers in cardiovascular medicine · 2022
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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

6 authors at 2 institutions in 1 country.

Jin YanHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, 610072, Sichuan Province, P.R. China.
Disi DengHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, 610072, Sichuan Province, P.R. China.
Yeke WuDepartment of Stomatology, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, 610072, Sichuan Province, P.R. China.
Keming WuDepartment of Gynaecology, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, 610072, Sichuan Province, P.R. China.
Jie QuShaanxi University of Chinese Medicine, Xianyang 712046, Shaanxi Province, P.R. China.
Fei LiShaanxi University of Chinese Medicine, Xianyang 712046, Shaanxi Province, P.R. China.
Shaanxi University of Chinese Medicine · CNStomatology Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disrupted follicular development may result in increased follicular atresia, which is a crucial mechanism of various ovarian pathologies. It has been demonstrated that oxidative stress is associated with disrupted follicular development. Catalpol is a natural compound that has been found to possess antioxidative stress. However, the effects of catalpol on oxidative stress-induced disrupted follicular development remain unclear. In the present study, we evaluated the protective effect of catalpol on hydrogen peroxide (H2O2)-induced oxidative damage in granulosa cells (GCs), which play crucial roles in the follicular development. Our results showed that catalpol significantly improved cell viability, reduced reactive oxygen species (ROS) and malondialdehyde (MDA) production, and elevated superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities in H2O2-induced GCs. Catalpol treatment caused significant increase in bcl-2 expression, and decreases in bax and caspase-9 expressions. Compared with the H2O2-induced GCs, caspase-3 activity in catalpol-treated cells was markedly decreased. Furthermore, catalpol caused significant activation of PI3K/Akt/mTOR pathway in GCs in response to H2O2 stimulation. Additionally, inhibition of this pathway reversed the inhibitory effects of catalpol on H2O2-induced oxidative injury and apoptosis in GCs. In conclusion, these findings suggested that catalpol protected GCs from H2O2-induced oxidative injury and apoptosis via activating PI3K/Akt/mTOR signaling pathway. Thus, catalpol might serve as a therapeutic approach for regulating disrupted follicular development.

Indexed as

AnimalsApoptosisCells, CulturedFemaleGranulosa CellsHydrogen PeroxideIridoid GlucosidesModels, AnimalOxidative StressPhosphatidylinositol 3-KinasesPrimary Cell CultureProto-Oncogene Proteins c-aktRatsSignal TransductionTOR Serine-Threonine KinasesAkt1 protein, ratcatalpolHydrogen PeroxideIridoid GlucosidesmTOR protein, ratPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinasesapoptosiscatalpoldisrupted follicular developmentgranulosa cells (GCs)oxidative stressPI3K/Akt/mTOR signaling pathway

Identifiers

PMID32227125
PMCPMC7167250
OpenAlexW3013333277

What OpenQuestion holds

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LicenceCC BY
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.