Evidence map›Paper›PMID 39880748›Full record

ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2025

Spatial metabolic analysis of the regulatory effects of DL-3-n-butylphthalide in a cerebral ischemia-reperfusion mouse model.

Yuxuan Lu, Jianwen Deng, Yining Huang, Jingjing Jia, Qing Peng, Ran Liu, Zhiyuan Shen, Weiping Sun, Haiqiang Jin, Zhaoxia Wang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

10 authors.

Yuxuan LuDepartment of Neurology, Peking University First Hospital, Beijing, China.
Jianwen DengDepartment of Neurology, Peking University First Hospital, Beijing, China.
Yining HuangDepartment of Neurology, Peking University First Hospital, Beijing, China.
Jingjing JiaDepartment of Neurology, Peking University First Hospital, Beijing, China; Department of Neurology, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing, China.
Qing PengDepartment of Neurology, Peking University First Hospital, Beijing, China.
Ran LiuDepartment of Neurology, Peking University First Hospital, Beijing, China.
Zhiyuan ShenDepartment of Neurology, Peking University First Hospital, Beijing, China; Department of Neurology, The First Hospital of Hebei Medical University, Shijiazhuang, China.
Weiping SunDepartment of Neurology, Peking University First Hospital, Beijing, China.
Haiqiang JinDepartment of Neurology, Peking University First Hospital, Beijing, China. Electronic address: jhq911@bjmu.edu.cn.
Zhaoxia WangDepartment of Neurology, Peking University First Hospital, Beijing, China. Electronic address: drwangzx@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DL-3-n-butylphthalide (NBP) exhibits promising pharmacological efficacy against ischemia-reperfusion injury, but its protective effects may involve many mechanisms that are yet to be fully understood. This study aimed to profile the metabolic alterations induced by NBP during the process of ischemia-reperfusion using spatial metabolomics. Our study found that NBP could significantly reduce the ischemic area and restore physical function by potentially modulating pathways of the citrate cycle, pyruvate metabolism, autophagy, and unsaturated fatty acid biosynthesis. During the process of ischemia-reperfusion, NBP played a therapeutic role in improving energy supply, decreasing autophagy, and improving unsaturated fatty acid biosynthesis. Subsequent studies confirmed improvements in relevant indices of mitochondrial morphology, autophagy, and ferroptosis after treatment with NBP. These findings shed light on novel mechanisms underlying the efficacy of NBP in treating cerebral ischemia/reperfusion injury associated with ischemic stroke.

Indexed as

BenzofuransBrain IschemiaNeuroprotective AgentsReperfusion InjuryAnimalsAutophagyDisease Models, AnimalMaleMetabolomicsMiceMice, Inbred C57BL3-n-butylphthalideBenzofuransNeuroprotective AgentsDL-3-n-butylphthalideIn situIschemia-reperfusion injurySpatial metabolomics

Identifiers

PMID39880748
PMCPMC12014401

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.