Neuroprotective effect of Clerodendron glandulosum against acute transient ischemia reperfusion cerebral injury in rats

Cerebral ischemia is a condition in which there is insufficient blood flow to the brain to meet metabolic demands. This leads to poor oxygen supply or cerebral hypoxia and thus leading to the death of brain tissues or cerebral infraction/ischemia stroke. It has been third most common cause of death in developed countries, Stroke can affect walking, talking, speech, vision, spatial awareness, swallowing, bladder control, bowel control and balance co-ordination. Free radical formation has been proved during cerebral ischemia. Risk factors for stroke include advanced age, hypertension, transient ischemic attack, diabetes; high cholesterol, cigarette smoking and atrial fibrillation. Among stroke patients, 80% suffer from cerebral infraction and 20% from cerebral haemorrhage [1,2]. Several components of reactive oxygen species (ROS) (superoxide, hydroxyl radical, hydrogen peroxide and peroxynitrite radical) that are generated after ischemia reperfusion injury play an important role in neuronal loss after cerebral ischemia [3]. In reperfusion injury arrivals of oxygen to the ischemia area following restoration of blood flow instead of alleviating ischemic state worsens damage. Xanthine oxidase (XO) is major factor in generation of superoxide radical has been consider to play an important role in genesis of tissue injury due to ischemia and reperfusion. There is evidence that XO levels are elevated during ischemia. XO is the first known O2 radical source. During ischemia, adenosine triphosphate is degraded to hypoxanthine and xanthine dehydrogenase is converted to XO. During reperfusion, XO catalyses the conversion of hypoxanthine to uric acid with release of O2 radical [3]. Nitric oxide synthase (iNOS) is up regulated after reperfusion injury. This results in excessive nitric oxide (NO) production. However some reports suggested that NO inhibits XO activity. Many antioxidants are reported to reduced reactive oxygen species-mediated reaction and protect neurons from ischemia-reperfusion induced neural loss in animal models of cerebral ischemia [4-6]. Cerebral ischemia leads to inflammatory cells which releases inflammatory cytokines and Cerebral ischemia may be due to primary thrombosis in carotid artery. This results in cerebral hypoxia and thus leading to cerebral infarction/ischemic stroke. The effect of CGE (C. glandulosum extract) on antioxidant status in I/R (ischemia-reperfusion) injury in the rat forebrain have been investigated. Further, its effect was assessed on behavioural parameters, infract size and histopathological parameters. Bilateral carotid artery occlusion followed by reperfusion produced significant cerebral infarction and impaired short term memory, motor co-ordination and lateral push response CGE markedly attenuated I/R induced cerebral injury in terms of decreased infarct, size. The result suggests that the use of CGE protect ischemia reperfusion induced cerebral injury with comparable potency. Abstract Neuroprotective effect of Clerodendron glandulosum against acute transient ischemia reperfusion cerebral injury in rats.