Evidence map›Paper›PMID 36909944›Full record

ArticleFrontiers in aging neuroscience2023

Neuroprotective effect of Dl-3-n-butylphthalide against ischemia-reperfusion injury is mediated by ferroptosis regulation

Shuangli Xu, Xuewei Li, Yutian Li, Xiangling Li, E Lv, Xiaojun Zhang, Youkui Shi, Yanqiang Wang

Abstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

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  11. International journal of molecular sciences · 2024
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  12. Cerebroprotective action of butylphthalide in acute ischemic stroke: Potential role of Nrf2/HO-1 signaling pathway.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
    Article
  13. Butylphthalide inhibits ferroptosis and ameliorates cerebral Ischaemia-Reperfusion injury in rats by activating the Nrf2/HO-1 signalling pathway.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
    Article
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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

8 authors.

Shuangli XuEmergency Department, The Affiliated Hospital of Weifang Medical University, Weifang, Shandong, China.
Xuewei LiDepartment of Rheumatology, The Affiliated Hospital of Weifang Medical University, Weifang, Shandong, China.
Yutian LiSchool of Pharmacy, Weifang Medical University, Weifang, Shandong, China.
Xiangling LiDepartment of Internal Medicine, The Affiliated Hospital of Weifang Medical University, Weifang, Shandong, China.
E LvDepartment of Histology and Embryology, Weifang Medical University, Weifang, Shandong, China.
Xiaojun ZhangDepartment II of Neurology, The Affiliated Hospital of Weifang Medical University, Weifang, Shandong, China.
Youkui ShiEmergency Department, The Affiliated Hospital of Weifang Medical University, Weifang, Shandong, China.
Yanqiang WangDepartment of Rheumatology, The Affiliated Hospital of Weifang Medical University, Weifang, Shandong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Stroke is one of the most severe diseases worldwide, resulting in physical and mental problems. Dl-3-n-butylphthalide, a compound derived from celery seed, has been approved for treating ischemic stroke in China. No study has evaluated how Dl-3-n-butylphthalide affects the ferroptosis SLC7A11/GSH/GPX4 signal pathway and blood-brain barrier (BBB) PDGFRβ/PI3K/Akt signal pathways in the rat middle cerebral artery occlusion/reperfusion (MCAO/R) model of ischemic stroke. Methods: Sprague-Dawley rats were used to develop the MCAO/R model. Our study used three incremental doses (10, 20, and 30) of Dl-3-n-butylphthalide injected intraperitoneally 24 h after MCAO/R surgery. The neuroprotective effect and success of the model were evaluated using the neurofunction score, brain water content determination, and triphenyl-tetrazolium chloride-determined infarction area changes. Pathological changes in the brain tissue and the degree of apoptosis were examined by hematoxylin and eosin, Nissl, and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. In addition, pathway proteins and RNA expression levels were studied to verify the effects of Dl-3-n-butyphthalide on both pathways. At the same time, commercial kits were used to detect glutathione, reactive oxygen species, and malondialdehyde, to detect oxidative stress in brain tissues. Results: The middle dose of Dl-3-n-butylphthalide not only improved MCAO-induced brain dysfunction and alleviated pathological damage, brain inflammatory response, oxidative stress, and apoptosis but also protected against ferroptosis and reduced BBB damage. These changes resulted in improved neurological function in the cerebral cortex. Conclusion: We speculate that Dl-3-n-butylphthalide has a neuroprotective effect on focal cerebral ischemia/reperfusion, which may be mediated through ferroptosis-dependent SLC7A11/GSH/GPX4 signal pathway and PDGFRβ/PI3/Akt signal pathway.

Indexed as

blood–brain barrierferroptosisischemic/reperfusionN-butylphthalideneuroinflammation

Identifiers

PMID36909944
PMCPMC9995665

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Registered trials

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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.