SUN11602 Accelerates Early Peripheral Nerve Regeneration in an Experimental Median Nerve Transection Model

Peripheral nerve injury (PNI) is one of the common life-altering disabilities resulting in various degrees of impairment in movement and sensation alongside apraxia and long-lasting pain. The gold standard for restoring the transected nerves is bridging the distal and proximal ends of disrupted autologous nerve using neurosurgical sutures. This approach is helpful, however nerve bridging is valid in pay of consuming healthy nerves and scarring phenomena in damaged site besides difficult donor nerve accessibility and extra surgery is required. Many studies have demonstrated that bFGF plays a pivotal role in the regeneration of PNI and severe spinal cord injury, exerting neuroprotective activity by binding to fibroblast growth factor receptors (FGFRs). Particularly, bFGF exhibits a high affinity for the receptor FGFR1, serving as its specific ligand. The novel synthetic compound SUN11602 exhibited neuroprotective activities like bFGF. Therefore, this study aimed to evaluate the effect of SUN11602 treatment in a rat experimental model of peripheral median nerve transection (MNT) and end-to-end suture. MNT was performed on rats, starting from 24 h following the surgical procedure, to orally treat, daily for 7 days, with SUN11602 at the dose of 2.5 mg/kg. The results showed that SUN11602 administration significantly reduced the alteration of PNI, promoting median nerve regeneration, suppressed mast cell accumulation, and resident macrophages. Also, SUN11602 reduced pro-inflammatory response of M1 macrophages, stimulated Schwann cell proliferation, and slowed down median nerve demyelination and fibrosis. Therefore, SUN11602 could be considered a valuable pharmacological strategy for MNT.