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Updated: Jan 20, 2026
PI3K/mTOR/AKT Signaling Pathway
Catalpol may improve axonal growth via regulating miR-124 regulated PI3K/AKT/mTOR pathway in neurons after ischemia
Huifeng Zhu1, Jinghuan Wang1, Yali Shao1
1College of Pharmaceutical Sciences & Chinese Medicine, Southwest University, Chongqing 400716, China.
Background:
MicroRNA-124 (miR-124) is a brain-specific miRNA molecule, the highest expression in the cortex and is associated with neuronal protection after stroke. This study aimed to investigate whether catalpol could affect miR-124 to regulate PI3K/AKT/mTOR pathway, promoting axonal growth in stroke rats.
Methods:
Cells were divided into three groups: control group, miRNA124 agomir group, and miRNA124 antagomir group. To explore the mechanism, cells were divided into seven groups: control group, OGD group (OGD/R), miRNA124 agomir group, miRNA124 agomir plus catalpol group, miRNA124 antagomir group, miRNA124 antagomir plus catalpol group, and catalpol group. Before OGD/R, miRNA124 antagomir and microRNA124 agomir were transfected into neurons for 6 h by using ribo FECT nd Consumablesn/reper transfection kit. Cell survival and cell death were detected by MTT and LDH assay. Axonal growth was assessed by MAP-2 immunofluorescence staining. Western blotting and qPCR were used to detect the expression of molecules in the PI3K/AKT/mTOR pathway.
Results:
Inhibition of miR-124 activated PI3K/AKT/mTOR pathway and promoted neuronal survival and axonal growth. The expression of miR-124 increased after OGD/R, and catalpol could inhibit miR-124 to activate PI3K/AKT/mTOR pathway to further promote axonal growth.
Conclusions:
It is concluded that catalpol may inhibit miR-124 to activate PI3K/AKT/mTOR pathway, promoting axonal growth.
Insights
Catalpol inhibits microRNA-124 (miR-124), activating the PI3K/AKT/mTOR pathway. This promotes neuronal survival and axonal growth in stroke models.
Area of Science:
- Neuroscience
- Molecular Biology
- Pharmacology
Background:
- MicroRNA-124 (miR-124) is a brain-specific molecule crucial for neuronal protection post-stroke.
- Its highest expression is observed in the cortex.
Purpose of the Study:
- Investigate catalpol's effect on miR-124.
- Determine if catalpol regulates the PI3K/AKT/mTOR pathway via miR-124.
- Assess promotion of axonal growth in stroke rats.
Main Methods:
- Neuronal cultures subjected to oxygen-glucose deprivation/reoxygenation (OGD/R).
- Transfection with miR-124 agomir/antagomir.
- Assessment of cell survival, death, and axonal growth (MAP-2 staining).
- Detection of PI3K/AKT/mTOR pathway molecules via Western blotting and qPCR.
Main Results:
- Inhibition of miR-124 activated the PI3K/AKT/mTOR pathway, enhancing neuronal survival and axonal growth.
- OGD/R increased miR-124 expression.
- Catalpol inhibited miR-124, activating the PI3K/AKT/mTOR pathway and promoting axonal growth.
Conclusions:
- Catalpol inhibits miR-124, thereby activating the PI3K/AKT/mTOR pathway.
- This mechanism promotes axonal growth, offering a potential therapeutic strategy for stroke recovery.
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