Evidence map›Paper›PMID 38010098›Full record

ArticleBrain and behavior2023

Gandouling alleviates nerve injury through PI3K/Akt/FoxO1 and Sirt1/FoxO1 signaling pathway to inhibit autophagy in the rats model of Wilson's disease.

Li Chen, Wangyang Xu, Yuting Zhang, Hao Chen, Yanquan Han

Open access · goldAbstract read
In one paragraph

Article in Brain and behavior, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 11 citations in OpenAlex.

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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

5 authors at 1 institution in 1 country.

Li ChenInstitute of Pharmaceutical Department, The First Affiliated Hospital of Anhui University of Traditional Chinese Medicine, Hefei, P. R. China.ORCID 0000-0002-6932-4068
Wangyang XuInstitute of school of pharmacy, Anhui University of Chinese Medicine, Hefei, P. R. China.
Yuting ZhangInstitute of Pharmaceutical Department, The First Affiliated Hospital of Anhui University of Traditional Chinese Medicine, Hefei, P. R. China.
Hao ChenInstitute of Pharmaceutical Department, The First Affiliated Hospital of Anhui University of Traditional Chinese Medicine, Hefei, P. R. China.
Yanquan HanInstitute of Pharmaceutical Department, The First Affiliated Hospital of Anhui University of Traditional Chinese Medicine, Hefei, P. R. China.
Anhui University of Traditional Chinese Medicine · CN

Funding

The Key Research and Development Projects of Anhui Province 202004j07020048
6 · The paper itself

Abstract

introductionPrevious studies have shown that Gandouling (GDL) may alleviate the nerve damage caused by Wilson's disease (WD) by inhibiting the autophagy of nerve cell mitochondria. However, its mechanisms are still unclear. Revealing the therapeutic mechanism of GDL is beneficial for its clinical application and provides theoretical support for the development of new formulations for treating WD.

methodThis time we found that the oxidative stress level in the body of the copper-overloaded WD rates increased, neurons in the hippocampus were damaged, and autophagy occurred. GDL reversed these situations and significantly improved the learning, memory, and spatial cognitive abilities of the high-copper-loaded WD rates. After GDL intervention, the expression of phosphatidylinositol-3 kinase (PI3K), phosphorylated serine-threonine protein kinase (AKT), and phosphorylated forkhead box protein O1 (FoxO1) significantly increased, whereas FoxO1 in the nucleus decreased and phosphorylated FoxO1 in the cytoplasm also significantly raised. In addition, the expression of Sirt1 significantly declined, and Ac-FoxO1 in the nucleus also significantly increased.

resultsThese data indicated that GDL may promote the phosphorylation of FoxO1 and promote its nucleation by activating the PI3K/AKT/FoxO1 signaling pathway and inhibit Ac-FoxO1 hydrolysis in the nucleus through the Sirt1/FoxO1 signaling pathway to suppress the transcriptional activity of FoxO1.

conclusionFurthermore, it inhibited the expression of autophagy genes Atg12 and Gabarapl1. In summary, our work provides new insights into the potential mechanisms of GDL repairing WD neuronal damage through autophagy pathways.

Indexed as

Hepatolenticular DegenerationPhosphatidylinositol 3-KinaseAnimalsAutophagyCopperForkhead Box Protein O1Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsSignal TransductionSirtuin 1CopperForkhead Box Protein O1Phosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSirt1 protein, ratSirtuin 1Gandoulingnerve injurysignaling pathwayWilson disease

Identifiers

PMID38010098
PMCPMC10726812
OpenAlexW4389069790

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.