Effects of saffron [Crocus sativus L.] stigma extract and its active constituent crocin on neuropathic pain responses in a rat model of chronic constriction injury

This study was designed to investigate the therapeutic effects of saffron [Crocus Sativus L] and its main constituent crocin on neuropathic pain behavioral responses induced by chronic constriction injury [CCI] in rats. Adult male Wistar rats [200 to 250 g] were randomly assigned into 5 groups: Sham + saline, CCI + saline, CCI+ saffron [30 mg/kg], CCI +crocin [15 mg/kg] and CCI + crocin [30 mg/kg]. CCI was induced by applying 4 loose ligatures around the sciatic nerve. Two weeks after nerve lesion, injections of saline, saffron or crocin were started and continued until 26th day post-surgery. Pain behavioral responses including mechanical allodynia [von Frey filament testing] and thermal hyperalgesia were measured in 14, 17, 20, 23, 26, and 40th days after CCI. CCI significantly increased pain behavioral responses. Saffron and crocin [30 mg/kg] decreased thermal hyperalgesia and mechanical allodynia on day 26, and this effect continued until the day 40. Crocin at lower dose [15 mg/kg] was ineffective. These findings indicate that treatment of saffron and crocin after CCI may have a therapeutic effect against neuropathic pain, suggesting that these substances may offer new strategies for the treatment of this highly debilitating condition

Effects of aminoguanidin on the neuropathic behavioral responses of chronic constriction injury model in rat

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