Gelatine nanostructured lipid carrier encapsulated FGF15 inhibits autophagy and improves recovery in spinal cord injury

Cell Death Discovery, 2020 · DOI: https://doi.org/10.1038/s41420-020-00367-y · Published: December 1, 2020

Simple Explanation

This study explores the potential of using gelatine nanostructured lipid carriers (GNLs) to deliver fibroblast growth factor 15 (FGF15) for treating spinal cord injuries (SCI). The researchers compared the effects of FGF15 alone versus FGF15 encapsulated in GNLs on SCI recovery in rats. The study found that FGF15-GNLs enhanced repair after SCI compared to FGF15 alone. This was linked to the suppression of autophagy, a cellular process where cells degrade their components, and the reduction of glial scar formation, which inhibits nerve regeneration. These findings suggest that FGF15-GNLs have therapeutic potential for treating SCI by inhibiting autophagy, reducing glial scarring, and promoting nerve regeneration.

Study Duration

Not specified

Participants

Young adult female Sprague–Dawley rats ~8 weeks of age (weighing 220–250 g)

Evidence Level

Not specified

Key Findings

1
FGF15-GNLs significantly improved hindlimb locomotor function in rats with SCI compared to FGF15 alone, as measured by the BBB locomotion scale.
2
FGF15-GNLs treatment resulted in a significant reduction in necrosis, karyopyknosis, and immune cell infiltration in spinal cord tissue after SCI, indicating neuroprotection.
3
FGF15-GNLs inhibited autophagy in SCI, as evidenced by decreased levels of LC3-II and beclin-1, and increased levels of p62, suggesting improved autophagy clearance.

Research Summary

This study investigated the therapeutic effects of gelatine nanostructured lipid carriers (GNLs) encapsulating fibroblast growth factor 15 (FGF15) in a rat model of spinal cord injury (SCI). The researchers compared the effects of FGF15-GNLs to FGF15 alone and a control group. The results showed that FGF15-GNLs significantly improved locomotor function, reduced tissue damage, and inhibited autophagy in the injured spinal cord compared to FGF15 alone. The treatment also reduced glial scar formation and promoted axon regeneration. The findings suggest that FGF15-GNLs have potential as a therapeutic strategy for SCI by promoting nerve regeneration and inhibiting autophagy-related cell death and glial scarring.

Practical Implications

Therapeutic Potential for SCI

FGF15-GNLs could be developed as a novel therapeutic agent for spinal cord injury, offering improved recovery outcomes compared to traditional treatments.

Targeting Autophagy

The study highlights the importance of autophagy modulation in SCI treatment, suggesting that therapies targeting autophagy pathways could be beneficial.

Drug Delivery System

GNLs demonstrate promise as an effective drug delivery system for neurotrophic factors, potentially improving their stability, bioavailability, and targeted delivery to the injured spinal cord.

Study Limitations

1
The study was conducted on a rat model, and further research is needed to confirm these findings in humans.
2
The long-term effects of FGF15-GNLs treatment on spinal cord regeneration and functional recovery were not fully evaluated.
3
The specific mechanisms by which FGF15-GNLs inhibit autophagy and promote nerve regeneration require further investigation.

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