Evidence map›Paper›PMID 40890801›Full record

ArticleChinese medicine2025

Houttuynia cordata Thunb-derived extracellular vesicle-like particles alleviate ischemic brain injury by miR159a targeting ACSL4 to suppress ferroptosis.

ShenYang Zhang, ZhiYan Liang, ChunYi Wu, ZiLu Qin, XueWen Wei, YiNing Liu, RuiQi Su, LiLi Li, Bin Sun, LinYan Huang and 4 more

Abstract read
In one paragraph

Article in Chinese medicine, 2025. 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
–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

13 citing papers in PubMed.

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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

14 authors.

ShenYang Zhang *Department of Neurology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, People's Republic of China.
ZhiYan Liang *School of Medical Technology, Xuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou, 221004, Jiangsu, People's Republic of China.
ChunYi Wu *School of Medical Technology, Xuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou, 221004, Jiangsu, People's Republic of China.
ZiLu QinSchool of Medical Technology, Xuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou, 221004, Jiangsu, People's Republic of China.
XueWen WeiDepartment of Laboratory Medicine, Affiliated Xuzhou Municipal Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, People's Republic of China.
YiNing LiuSchool of Medical Technology, Xuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou, 221004, Jiangsu, People's Republic of China.
RuiQi SuSchool of Medical Technology, Xuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou, 221004, Jiangsu, People's Republic of China.
LiLi LiSchool of Medical Technology, Xuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou, 221004, Jiangsu, People's Republic of China.
Bin SunSchool of Medical Technology, Xuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou, 221004, Jiangsu, People's Republic of China.
LinYan HuangSchool of Medical Technology, Xuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou, 221004, Jiangsu, People's Republic of China.
Wan WangSchool of Medical Technology, Xuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou, 221004, Jiangsu, People's Republic of China.
JianGang ShenSchool of Chinese Medicine, The University of Hong Kong, Hong Kong SAR, Hong Kong, China.
GuangSheng WangDepartment of Neurology, The Affiliated Shuyang Hospital of Xuzhou Medical University, Shuyang, 223600, Jiangsu, People's Republic of China. 760020220454@xzhmu.edu.cn.
SuHua QiSchool of Medical Technology, Xuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou, 221004, Jiangsu, People's Republic of China. suhuaqi@xzhmu.edu.cn.ORCID http://orcid.org/0000-0002-1479-701X

Funding

the Grants of Natural Science Foundation of Jiangsu Province, China BK20211348the Jiangsu Provincial Health Commission Medical Research Project Z2023089the Leadership program at Xuzhou Medical University JBGS202203the Natural Science Foundation of the Jiangsu Higher Education Institutions of China 23KJB310025the Xuzhou Key Research and Development Plan KC23277
6 · The paper itself

Abstract

introductionNeuroprotective agents for acute ischemic stroke often fall short in efficacy due to the blood-brain barrier challenges, lack of target specificity, and limited effectiveness. Recently, plant-derived extracellular vesicle-like particles (EVLP) have shown promise in their multifaceted functions.

objectivesThe neuroprotective advantages that EVLP produced from Houttuynia cordata Thunb against cerebral ischemia/reperfusion injury are investigated.

methodsThe extraction of HT-EVLP was performed using gradient centrifugation and ultracentrifugation, followed by identification of its particle size, morphology, and exosomal marker proteins. Using behavioral tests and a rat model of middle cerebral artery occlusion (MCAO), the neuroprotective attributes of HT-EVLP were assessed. To evaluate the effect of HT-EVLP on ferroptosis and cell survival, the oxygen-glucose deprivation/reoxygenation (OGD/R) induced HT22 cell model was used. Utilizing bioinformatics analysis and small RNA sequencing, the miRNA composition and downstream target genes of HT-EVLP were predicted. The dual-luciferase reporter gene assay was used to confirm that miR159a bound to long-chain acyl-coenzyme A synthase 4 (ACSL4). The impact of miR159a transfection on OGD/R-induced ferroptosis in HT22 cell was also observed.

resultsUsing a MCAO model, we found that HT-EVLP preserved blood brain barrier integrity, naturally penetrated the infarct core area, reduced cerebral infarct volume, mitigated neuronal apoptosis and ferroptosis, and facilitated recovery of neuronal function. In vitro studies further revealed that HT-EVLP enhanced cell survival and suppressed ACSL4-mediated ferroptosis in OGD/R-treated HT22 cells. Small RNA sequencing indicated that HT-EVLP are rich in miRNAs, with miR159a, among the top 10, potentially regulating ferroptosis-related pathways and directly binding to the 3'UTR of ACSL4. Overexpression of miR159a reduced Erastin-induced ACSL4 expression and alleviated mitochondrial damage in HT22 cells without causing toxicity.

conclusionsThis study highlights the potential of HT-EVLP as carriers of endogenous miR159a, offering a promising strategy for ischemic brain injury therapy.

Indexed as

ACSL4Cerebral ischemia–reperfusionFerroptosisHT-EVLPmiR159a

Identifiers

PMID40890801
PMCPMC12400549

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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.