RESUMO
Previous studies have shown that different mechanisms are involved in neuropathic pain. Increasing nitric oxide [NO] in the location of injury may be an effective factor in neuropathic pain which, in turn, acts through increasing membrane permeability. The aim of this study was to examine the effects of aminoguanidin, a specific inhibitor of inducible nitric oxide synthetase [iNOS] on neuropathic pain behaviors. Male Wistar rats [200-300 gram] were used. Chronic constriction injury [CCI] in the rats were produced by four loosely ligation that the distance between them is 1 millimeter before the triple branching of sciatic nerve. Two weeks later, the animals were tested for thermal hyperalgesia and mechanical allodynia. Aminoguanidine were injected [I.P] 60 min before test in doses of 75, 150 and 300 mg/kg. Our studies showed CCI induced neuropathic pain in all rats. All doses of aminoguanidin [75, 150, 300 mg/kg] significantly reduced mechanical allodynia and thermal hyperalgesia in compared with CCI group. Moreover, the effect of aminoguanidin on thermal hyperalgesia at dose of 300 mg/kg was significantly higher than two lower doses. According to findings of this and other studies, aminoguanidin has an important influence in reducing neuropathic pain. This effect, at least in part, is mediated through inhibition of iNOS. Additionally, an inhibition of di-aminoxidase or anti oxidative effects may be contributed to inhibitory effects of aminoguanidin on neuropathic pain. Thus, further investigations can determine the mechanism of aminoguanidin effects in neuropathic Pain. Findings of this study open a new window for synthesis of new drugs for management of neuropathic pain in clinic