Evidence map›Paper›PMID 41689208›Full record

ArticleCNS neuroscience & therapeutics2026

Pachymic Acid Targets PI3K/Akt Signaling Pathway to Attenuate tPA-Induced Hemorrhagic Transformation After Ischemic Stroke.

Yongshi Wu, Tong Zhang, Ruoqi Li, Yige Wu, Congmin Wei, Fangming Sun, Shanshan Zhang, Xiang Fan

Abstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

8 authors.

Yongshi WuSchool of Basic Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, China.
Tong ZhangSchool of Basic Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, China.
Ruoqi LiSchool of Basic Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, China.ORCID 0000-0002-8343-6787
Yige WuSchool of Basic Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, China.
Congmin WeiSchool of Basic Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, China.
Fangming SunSchool of Basic Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, China.
Shanshan ZhangSchool of Basic Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, China.
Xiang FanSchool of Basic Medical Sciences, Zhejiang Chinese Medical University, Hangzhou, China.ORCID 0000-0001-7697-0378

Funding

Zhejiang Provincial Natural Science Foundation of China LY22H280004
6 · The paper itself

Abstract

backgroundTissue plasminogen activator (tPA)-induced cerebral hemorrhagic transformation (HT) after ischemic stroke limits its clinical use widely. Pachymic acid, a main active component of Poria cocos, mitigates brain ischemia/reperfusion injury, but its effect on tPA-induced HT is unclear.

methodsA focal middle cerebral artery occlusion/reperfusion model was established and administered with tPA and pachymic acid. Infarct volume and neurological function were assessed at 24 h after reperfusion. Blood-brain barrier (BBB) damage was evaluated using Evans blue leakage, immunofluorescence, and Western blot. Pachymic acid and PI3K protein interaction was identified using molecular docking, molecular dynamics (MD) simulation, and surface plasmon resonance (SPR).

resultsCompared with the tPA group, pachymic acid dose-dependently improves neurological and motor functions, reduces infarct volume and hemorrhagic volume, and alleviates permeability and tight junction protein degradation of BBB after ischemic stroke, with the strongest effects observed at the highest dose. Molecular docking, MD simulation, and SPR results indicate that pachymic acid can directly bind to PI3K protein. Further experiments showed that the PI3K inhibitor LY294002 reversed pachymic acid's protective effects.

conclusionsThis study demonstrated that pachymic acid protects the BBB by targeting PI3K to activate the PI3K/Akt signaling pathway, thereby alleviating tPA-induced HT after ischemic stroke.

Indexed as

Cerebral HemorrhageIschemic StrokePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionTissue Plasminogen ActivatorTriterpenesAnimalsBlood-Brain BarrierFibrinolytic AgentsInfarction, Middle Cerebral ArteryMaleMolecular Docking SimulationRats, Sprague-DawleyFibrinolytic Agentspachymic acidPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTissue Plasminogen ActivatorTriterpenesblood–brain barrierhemorrhagic transformationischemic strokePachymic acidPI3K/Akt signaling pathwaytPA

Identifiers

PMID41689208
PMCPMC12905004

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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.