Neuroprotective effect of vitamin E acetate in models of mononeuropathy in rats

Direct injury to a peripheral nerve causes an increase in free oxygen radicals, which can lead to tissue damage.Vitamin E is a major antioxidant used clinically and its study in nerve injury models has not been encounteredin the literature. The objective was to study the neuroprotective actions of vitamin E acetate 50 mg/kg byusing partial sciatic nerve ligation and sciatic nerve crush injury models in wistar rats. The parameters usedwere thermal hyperalgesia, motor function test and motor nerve conduction velocity. A steady improvement inthermal hyperalgesia was seen in vitamin E treated animals on day 8th (7.96±0.18 s) and day 7th (8.26±0.15 s)in the models of partial sciatic nerve ligation and sciatic nerve crush injury respectively. There was a reductionin pain which was observed behaviorally in motor function test in both the models and also was observed animprovement in motor nerve conduction velocity of vitamin E treated animals which steadily increased on15th day (31.59±1.41 m/s) and 30th day (39.29±2.07 m/s). These findings indicate that vitamin E acetate has apromising neuroprotective action in treating hyperalgesia and also improving conduction velocity in the modelof nerve ligation and nerve crush injury in rats.