Abstract
Neuropathic pain is a severe and unbearable condition which arises due to activation
of peripheral nociceptors after tissue damage, neuropathic pain is caused from anomalous
physiology of central or peripheral nervous system and it may not be related to the
ongoing tissue damage or inflammation. Involvement of oxidative damage has been reported
in the pathophysiology of neuropathic pain. The purpose of this study was to examine
the effect of lycopene to quench the free radicals produced as a result of the increased
oxidative stress in neuropathic pain. Neuropathic pain was induced in wistar rats
by partial sciatic nerve ligation. The effect was evaluated by assessing various behavioral
parameters (thermal hyperalgesia, cold hyperalgesia), biochemical parameters (lipid
peroxidation, reduced glutathione, superoxide dismutase and catalase) as well as histopathological
parameters in sciatic nerve. During the experiment group of 8 rats each was administered
drugs once daily intraperitonealy (I.P.) and naïve groups, sham group and sciatic
nerve ligated group were treated with vehicle for the duration of 14 days. Partial
sciatic nerve ligation (PSNL) significantly caused thermal hyperalgesia, cold hyperalgesia
and oxidative damage compared to normal and sham groups. Daily administration of lycopene
(25 mg/kg, 50 mg/kg) and gabapentin (100 mg/kg) considerably reversed hyperalgesia,
cold hyperalgesia and attenuated oxidative stress when compared to control group.
There was significant histological improvement in the in the architecture of myelinated
and unmyelinated fibers. The results indicated that free radical generation mechanism
might be involved in PSNL induced behavior, biochemical and histopathological changes
in wistar rats.
Key words lycopene - gabapentin - catalase - hyperalgesia - histopathological
