Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Thursday, September 25, 2025

Pharmacological mechanisms and therapeutic potential of Puerarin in post-stroke rehabilitation: Insights from network pharmacology and experimental validation

 

Will your competent? doctor and hospital ensure human testing gets done? NO? So, NOTHING RESEMBLING COMPETENCE ANYWHERE IN YOUR STROKE HOSPITAL? RUN AWAY!

Pharmacological mechanisms and therapeutic potential of Puerarin in post-stroke rehabilitation: Insights from network pharmacology and experimental validation


https://doi.org/10.1016/j.bbrc.2025.152610Get rights and content
Under a Creative Commons license
Open access

Highlights

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    Puerarin enhances angiogenesis and endothelial function after stroke.
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    Network pharmacology and docking identified key HIF-1α/VEGF targets.
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    In vitro assays confirmed activation of angiogenic signaling pathways.
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    A biphasic dose response underscores the need for optimal dosing.

Abstract

Background

Stroke is a leading cause of disability, and promoting post-stroke recovery through endothelial regeneration and angiogenesis is crucial for improving patient outcomes. Puerarin, a flavonoid derived from Pueraria lobata, has shown promise in enhancing angiogenesis and endothelial function. This study investigates the pharmacological mechanisms of Puerarin in post-stroke rehabilitation through network pharmacology and experimental validation.

Methods

Network pharmacology was used to identify potential gene targets of Puerarin and their association with post-stroke sequelae. A Venn diagram analysis identified 116 common targets. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed to identify enriched pathways. Molecular docking simulations were used to confirm interactions between Puerarin and key targets. Additionally, in vitro experiments using human umbilical vein endothelial cells (HUVECs) exposed to oxygen-glucose deprivation/re-oxygenation (OGD/R) were conducted to assess Puerarin's effects on cell migration, proliferation, and angiogenesis.

Results

Network pharmacology revealed several key pathways, with the HIF-1α/VEGF signaling pathway identified as a critical target. Experimental validation confirmed that Puerarin enhanced endothelial cell migration, proliferation, and angiogenesis in a concentration-dependent manner. At lower concentrations, Puerarin promoted angiogenesis and endothelial migration. Molecular docking simulations demonstrated favorable binding interactions between Puerarin and key angiogenic targets.

Conclusions

Puerarin may serve as a therapeutic agent for post-stroke rehabilitation, promoting vascular regeneration through endothelial cell migration and angiogenesis. Its ability to activate the HIF-1α/VEGF pathway underscores its potential in improving functional recovery. Further in vivo studies are required to optimize dosing, assess long-term efficacy, and explore clinical applications.

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