A76 Therapeutic potential of β-carotene hydrogels in sciatic nerve axotomy induced neuropathic pain in rats via fibroblast growth factor-13 activation in rat

<h3>Introduction</h3> Neuropathic pain mainly occurs due to alteration of neuronal micro-tubular proteins and glial cells. Retinoids possess the wound repair processes via fibroblast growth factor (FGF) regulatory actions. However, the role of β-carotene hydrogels (BCHG) in the amelioration of sciatic nerve repairs is not explored in rats. <h3>Aim of study</h3> The present study is designed to investigate the BCHG effect in sciatic nerve axotomy-induced neuropathic pain behaviour in rats with the connection of FGF-13 function. <h3>Method</h3> The axotomy of the sciatic nerve (SCT) was made in the sciatic nerve bifurcation site. The BCHG (20 μL of 2.5 and 5%), pregabalin (PG: 20 μL of 1%), and heparin-based hydrogel (HHG: 20 μL of 3%) were loaded in chitosan/keratin (CK) tube. The sciatic nerve functional index (SFI) was analyzed for neuronal functions. The pain-sensitive tests, i.e., thermal and mechanical hyperalgesia were assessed on the different days, i.e., days 0, 1, 7, 14, and 21. The tissue total protein, total calcium, tumor necrosis factor-alpha (TNF-α), and FGF-13 levels were estimated to assess tissue biomarker changes. <h3>Results</h3> The application of BCHG (2.5 and 5%) improves the neuronal repair process in SCT in rats via regulation of neuronal calcium, TNF-α, and FGF-13 protein expressions. It is also revealed in the neuropathic pain behaviour &amp; neuronal functional test. <h3>Conclusion</h3> Hence, the BCHG possesses neuronal repair actions in rat SCT and attenuates the neuropathic pain behaviours via FGF-13 activation, anti-TNF-α, and calcium channel regulatory actions. <h3>Conflict of Interest</h3> No