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

Introduction It is now very well known that events like nerve ligation directly causes mechanical injury to the nerve and symptoms produced in such animals resemble the symptoms produced in causalgia in humans. The animal model mimics both hyperalgesia (increased response to noxious stimuli) and allodynia (pain response to low threshold stimulus) [1–4]. Furthermore, it is also reported that extent of nerve trapped in the ligature also affects the effects elicited post surgery and most importantly the pain so produced post operatively is like burning sensation similar to burning sensation in causalgic humans [3,5,6]. Direct mechanical injury or ischemia or both can cause acute endothelial injury that can result in endothelial edema, agranulocyte plug or microvascular thrombosis. These factors interrupt the reflow and can cause continuous fiber injury. Moreover, endoneural edema may develop due to microvascular compression. Toxic substances released from neutrophils and macrophages after injury can impair tissue protection in normal conditions and permit the accumulation of free oxygen radicals which increase tissue destruction and cause tissue damage [5]. Reactive oxidant species (ROS) are critically involved in the development and maintenance of neuropathic pain. Studies suggest that systemic administration of non-toxic doses of free radical scavengers could be useful for treatment of neuropathic pain [7]. Also deficiency of some vitamins in the diet could lead to neuropathic pain [8]. Vitamin E (VE) is considered the most effective liposolouble antioxidant found in the human biological system. It interacts with free radicals and prevents lipid peroxidation [9,10]. Clinically, VE supplementation led to electrophysiological recovery of sensory conduction and evoked potentials [11]. Also VE supplementation in cancer patients showed that VE may have an important neuroprotective effects [12]. The objective of the study was to evaluate anti-hyperalgesic and neuroprotective effect of vitamin E acetate (50 mg/ kg, O.D.) after sciatic nerve lesion produced by partial sciatic nerve ligation and sciatic nerve crush injury in rats.