FGF10 Enhances Peripheral Nerve Regeneration via the Preactivation of the PI3K/Akt Signaling-Mediated Antioxidant Response

Frontiers in Pharmacology, 2019 · DOI: 10.3389/fphar.2019.01224 · Published: October 16, 2019

Pharmacology Regenerative Medicine Neurology

Simple Explanation

This study investigates how Fibroblast Growth Factor 10 (FGF10) affects nerve regeneration and recovery after peripheral nerve injury (PNI). The study found that administering FGF10 promotes axonal regeneration and functional recovery. FGF10 treatment prevents Schwann cells (SCs) from excessive oxidative stress-induced apoptosis, which is linked to the activation of phosphatidylinositol-3 kinase/protein kinase B (PI3K/Akt) signaling. The researchers suggest that FGF10 shows promise as a therapeutic drug for repairing sciatic nerve damage by reducing oxidative stress-induced apoptosis in SCs.

Study Duration

28 days

Participants

Male SD rats (200~220 g)

Evidence Level

Not specified

Key Findings

1
FGF10 continuously enhances the recovery of locomotor and sensory function in acute PNI.
2
FGF10 promotes axonal regeneration, as determined by histological evaluation, showing remarkably regenerated and regular nerve fibers in the FGF10-treated group.
3
FGF10 enhances the expression of functional proteins after sciatic nerve injury, upregulating the functional expression of S100, MPZ and PCNA.

Research Summary

The study demonstrates a novel role for FGF10 in improving sensory and motor functional recovery, enhancing axonal regrowth and remyelination, and increasing the expression of functional proteins after traumatic PNI. FGF10-induced neuroprotection and neuranagenesis is associated with attenuating the acute activation of oxidative stress and apoptosis in SCs, which is likely regulated by the activation of PI3K/Akt signaling. The research suggests that FGF10 may be considered a potential therapeutic agent for peripheral nerve reconstruction after injury, offering a new avenue for treatment.

Practical Implications

Therapeutic Potential

FGF10 may be a potential therapeutic agent for peripheral nerve reconstruction after injury.

Underlying Mechanism

FGF10-induced neuroprotection is linked to the activation of PI3K/Akt signaling.

Clinical Applications

The research may provide an alternative therapeutic strategy for utilizing FGF10 for treating acute traumatic PNI.

Study Limitations

1
The precise mechanisms of FGF10 action require further investigation.
2
The long-term effects of FGF10 treatment need to be evaluated.
3
The study was conducted on rats, and results may not directly translate to humans.

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