Partial role of multiple pathways in infarct size limiting effect of quercetin and rutin against cerebral ischemia-reperfusion injury in rats.

BACKGROUND Reperfusion therapy used in the treatment of cerebral ischemia often causes reperfusion neurological injury. Multiple pathological processes are involved in this injury including oxidative stress and components of the inflammatory response appear to play key roles in these deleterious effects. Thus new therapeutic strategies aimed at neutralization of OS-induced neurotoxicity support the application of natural antioxidant bioflavonoids. Both experimental and epidemiological evidence demonstrate that bioflavonoid such as quercetin and rutin are neuroprotective in models of cerebral ischemia reperfusion injury. However, recent studies indicate that the radical scavenger property of quercetin and rutin is unlikely to be the only reason for their cerebroprotective actions and in fact, a wide spectrum of cellular signaling events may well account for their biological actions. AIM In this study we attempted to establish the various mechanisms involved in the cerebroprotective activity of quercetin and rutin. METHODS Adult Sprague Dawely rats were anesthetized with thiopentone and subjected to global cerebral ischemia by occlusion of bicommon carotid arteries. Infarct size (TTC staining), SOD, MDA, CAT and MPO levels was assessed 4 h after the onset of ischemia. RESULTS Quercetin (50 mg/kg) and rutin (10 mg/kg) administered 10 min before reperfusion resulted in significant reduction of infarct size, MDA, and MPO levels and significant increase in SOD and CAT levels. Administration of L-NAME prior to administration of quercetin and rutin, significantly reduced the cerebroprotection offered by quercetin and rutin. CONCLUSIONS Possible partial role of antioxidant, anti-inflammatory and involvement of NO in the beneficial effects of bioflavonoids quercetin and rutin against cerebral ischemia reperfusion injury was observed.