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ArticleMetabolic brain disease2025

Mechanistic study of butylphthalide in alleviating cerebral Edema after intracerebral Hemorrhage by regulating miR-7-5p expression.

Xiqian Chen, Shige Wang, Qiang Lei, Jia Liu, Wei Lu

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Article in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

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1citing papers in PubMed, 1 pooled it
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1 · What the graph read from it

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 1 synthesis or guideline pooled it.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Xiqian Chen *Department of Neurology, Second Xiangya Hospital, Central South University, Changsha, China.
Shige Wang *School of Biological Science, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, England.
Qiang LeiDepartment of Neurology, Second Xiangya Hospital, Central South University, Changsha, China.
Jia LiuDepartment of Neurology, Second Xiangya Hospital, Central South University, Changsha, China.
Wei LuDepartment of Neurology, Second Xiangya Hospital, Central South University, Changsha, China. luwei0338@csu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the mechanisms by which butylphthalide (NBP) alleviates cerebral edema after intracerebral hemorrhage (ICH) through the regulation of miR-7-5p expression.

methodsAn ICH model was generated in CTX-TNA2 rat astrocyte cell lines using hemin intervention. An in vivo ICH model was created by injecting type IV collagenase into the basal ganglia of Sprague-Dawley (SD) rats. The cell/rat models were treated with NBP and/or stattic. The expression of STAT3, miR-7-5p, EGFR, PI3K, AKT, p-AKT, AKT2, AKT3, and AQP4 were assessed using qRT-PCR, Western blotting, and immunofluorescence. Brain water content was measured using the wet-to-dry weight method, and neurological deficits were evaluated using the NSS (neurological severity score).

resultsIn both the CTX-TNA2 ICH model and the rat ICH model, miR-7-5p expression was significantly reduced, while STAT3, EGFR, AKT, p-AKT, AKT2, AKT3, and AQP4 expression were elevated compared to the blank/sham-operated group. NBP increased the expression of STAT3 and miR-7-5p, while reducing the expression of EGFR, AKT, p-AKT, AKT2, AKT3, and AQP4. NBP also decreased brain water content and improved NSS scores. STAT3 inhibition significantly reduced STAT3 and miR-7-5p expression, increased the expression of EGFR, PI3K, AKT, p-AKT, AKT2, AKT3, and AQP4, and elevated brain water content. NBP can reverse the downregulation of STAT3 and miR-7-5p expression, the upregulation of EGFR/PI3K/AKT axis and AQP4 expression, and the increase in brain water content induced by STAT3 inhibition.

conclusionNBP alleviates cerebral edema after ICH by upregulating STAT3 expression, thereby increasing miR-7-5p levels and inhibiting the EGFR/PI3K/AKT axis and AQP4 expression.

Indexed as

BenzofuransBrain EdemaCerebral HemorrhageMicroRNAsAnimalsAquaporin 4AstrocytesDisease Models, AnimalMaleProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleySignal TransductionSTAT3 Transcription Factor3-n-butylphthalideAquaporin 4BenzofuransMicroRNAsProto-Oncogene Proteins c-aktSTAT3 Transcription FactorButylphthalide (NBP)Cerebral edemaIntracerebral hemorrhage (ICH)MiR-7-5pSTAT3

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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.