Basic Fibroblast Growth Factor-Releasing Bioabsorbable Polyglycolic Acid Dura Mater Enhances Neural Progenitor Cell Proliferation and Neuroprotection After Brain Injury.

BACKGROUND

Traumatic brain injury harms health, causes disability, and burdens health care systems and economies. Although new treatments for brain injury have been developed, their therapeutic efficacy remains insufficient. Herein, we demonstrate the therapeutic efficacy of artificial dura mater with varying basic fibroblast growth factor (bFGF)-releasing capabilities using a brain injury model.

METHODS

Artificial dura mater of lower (FGF-L) and higher (FGF-H) bFGF-releasing capabilities was prepared via oxygen plasma treatment for polyglycolic acid nonwoven fabric followed by bFGF adsorption. Mice received either bFGF-releasing dura mater (FGF-L, FGF-H) or bFGF-free dura mater (FGF-C) at the site of the induced brain injury.

RESULTS

Neurological functions significantly improved in the FGF-L and FGF-H groups compared with those in the FGF-C group on Day 14. No significant difference was observed in the brain injury area between the FGF-C group and either the FGF-L or FGF-H group. The number of SRY-box transcription factor 2-positive cells in the cortex was significantly larger in the FGF-L and FGF-H groups than in the FGF-C group on Day 7. The terminal transferase dUTP nick-end labeling-positive cell ratio was significantly lower in the FGF-H group than in the FGF-C group on Day 14. The occludin-positive and ZO-1-positive cell ratios were significantly greater in the FGF-H group than in the FGF-C group on Day 14, suggesting improved blood-brain barrier integrity.

CONCLUSION

The bFGF-releasing dura mater enhanced neural progenitor cell proliferation, inhibited apoptosis and blood-brain barrier breakdown, and contributed to neurological function recovery in brain-injured mice.