Evidence map›Paper›PMID 37999884›Full record

ArticleMetabolic brain disease2024

Network pharmacology-based approach to understand the effect and mechanism of chrysophanol against cognitive impairment in Wilson disease.

Xiao-Yan Zhang, Xie Wang, Ting Ye, Nan Shao, Jie Wang, Biao Cai, Dao-Jun Xie

Abstract read
PubMed Publisher
In one paragraph

Article in Metabolic brain disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 27% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
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 at 1 institution in 1 country.

Xiao-Yan Zhang *School of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine, Hefei, Anhui, 230012, People's Republic of China.ORCID 0009-0002-9650-3800
Xie Wang *The First Clinical Medical College, Anhui University of Chinese Medicine, Hefei, Anhui, 230031, People's Republic of China.ORCID 0009-0003-6627-9702
Ting Ye *School of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine, Hefei, Anhui, 230012, People's Republic of China.ORCID 0000-0002-4400-5642
Nan ShaoSchool of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine, Hefei, Anhui, 230012, People's Republic of China.ORCID 0000-0003-4728-5202
Jie WangSchool of Nursing, Anhui University of Chinese Medicine, Hefei, Anhui, 230012, People's Republic of China.ORCID 0009-0002-2361-3750
Biao CaiSchool of Integrated Chinese and Western Medicine, Anhui University of Chinese Medicine, Hefei, Anhui, 230012, People's Republic of China.ORCID 0000-0002-3375-0073
Dao-Jun XieEncephalopathy Center, The First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, Anhui, 230031, People's Republic of China. daojunxie@ahtcm.edu.cn.ORCID 0009-0005-5277-6083
Anhui University of Traditional Chinese Medicine · CN

Funding

the National Natural Science Foundation of China 8845the Natural Science Project of Anhui University of Chinese Medicine 8846
6 · The paper itself

Abstract

Wilson disease (WD) is a rare hereditary copper metabolism disorder, wherein cognitive impairment is a common clinical symptom. Chrysophanol (CHR) is an active compound with neuroprotective effects. The study aims to investigate the neuroprotective effect of CHR in WD and attempted to understand the potential mechanisms. Network pharmacology analysis was applied to predict the core target genes of CHR against cognitive impairment in WD. The rats fed with copper-laden diet for 12 weeks, and the effect of CHR on the copper content in liver and 24-h urine, the learning and memory ability, the morphological changes and the apoptosis level of neurons in hippocampal CA1 region, the expression level of Bax, Bcl-2, Cleaved Caspase-3, p-PI3K, PI3K, p-AKT, and AKT proteins were detected. Network pharmacology analysis showed that cell apoptosis and PI3K-AKT signaling pathway might be the main participants in CHR against cognitive impairment in WD. The experiments showed that CHR could reduce the copper content in liver, increase the copper content in 24-h urine, improve the ability of the learning and memory, alleviate the damage and apoptosis level of hippocampal neurons, down-regulate the expression of Bax, Cleaved Caspase-3, and up-regulate the expressions of Bcl-2, p-PI3K/PI3K, p-AKT/AKT. These results suggested that CHR could alleviate cognitive impairment in WD by inhibiting cell apoptosis and triggering the PI3K-AKT signaling pathway.

Indexed as

AnthraquinonesCognitive DysfunctionHepatolenticular DegenerationAnimalsApoptosisbcl-2-Associated X ProteinCaspase 3CopperHumansNetwork PharmacologyPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsAnthraquinonesbcl-2-Associated X ProteinCaspase 3chrysophanic acidCopperPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktCHRCognitive impairment in WDIn vivo experimentNetwork pharmacologyPharmacological mechanisms

Identifiers

PMID37999884
OpenAlexW4388976074

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.