Effect of Melatonin on Peripheral Nerve Damage Resulting from Tibial Defect in Rats

Peripheral nerve damage (PNI) can cause demyelination, axonal degeneration and loss of motor sensory function. Melatonin with its antioxidative effect, has been reported to reduce scar formation in injury, take a role repair process by suppressing fibroblast proliferation the damaged area. It was aimed investigate effect melatonin peripheral relationship between S100 proteins angiogenic regulation. Wistar albino rats were divided into 3 groups. In Defect group, 6 mm tibial bone defect using motorized drill created kept immobile for 28 days. + graft allograft treatment applied administered group. All sacrified decapitation, skin tibia removed then fixed 10 % neutral buffered formalin embedded paraffin, sections examined under light microscopy. Defect+Graft enlargement occlusion vessels epineural sheath, thickening endoneural sheath mild hyperplasia schwannocytus (Schwann cells) remarkable. Defect+Graft+Melatonin tight regular, structures prominent Mild expression observed group fibers region schwannocytus. (10mg/kg), moderate areas where proliferated nerve-connective tissue sheaths reconstructed. VEGF endoneural, perineural connective negative blood vessel endothelial cells, but positive We conclude that application melatonin; oxidative stress decreases, increases, having influence on regulation signaling angiogenetic structuring.