Cerebroprotective effect of Eclipta alba against global model of cerebral ischemia induced oxidative stress in rats.

Oxidative stress is believed to contribute to neuronal damage induced by cerebral ischemia/reperfusion (I/R) injury. The present study was undertaken to evaluate the possible cerebroprotective and antioxidant effect of hydroalcoholic extract of Eclipta alba against global cerebral ischemia in the rat. Adult Wistar albino rats were treated with extract of Eclipta alba (250 and 500mg/kg/day, p.o.) for 10 days. The global cerebral ischemia-reperfusion injury was induced by occluding bilateral common carotid arteries (BCCA) for 30min, followed by 4h reperfusion. Quercetin (20mg/kg, i.p.) was used for the reference compound. After that, animals were sacrificed by decapitation, brain was removed, various biochemical estimations, cerebral edema, assessment of cerebral infarct size, and histopathological examinations were carried out. BCCA caused significant depletion in superoxide dismutase (SOD), glutathione peroxidase (GPx), reduced glutathione (GSH), catalase (CAT), glutahione-S-transferase (GST), glutathione ruductase (GR) and significant increase in malondialdehyde (MDA) in brain. Pretreatment with hydroalcoholic extract of Eclipta alba significantly reversed the levels of biochemical parameters and significantly reduced the edema and cerebral infarct size as compared to the ischemic control group. Eclipta alba at higher dose markedly reduced ischemia-induced neuronal loss of the brain. Reduction of cerebral edema, an early symptom of ischemia, is one of the most important remedies for reducing subsequent chronic neural damage in stroke. The results of the study show that Eclipta alba pretreatment ameliorates cerebral ischemia/reperfusion injury and enhances the antioxidant defense against BCCA occlusion induced I/R in rats; so it exhibits cerebroprotective property. HPLC fingerprint of hydroalcoholic extract of Eclipta alba was performed for conforming the coumestan present in the plant extract.

Mansoorali KP ，Prakash T ，Kotresha D ，Prabhu K ，Rama Rao N ... -  《-》

Neuroprotective activity of Matricaria recutita Linn against global model of ischemia in rats.

Traditionally, the whole plant is used for various diseases, including neuronal disorders. To evaluate the neuroprotective effect of Matricaria recutita L. against global cerebral ischemia/reperfusion (I/R) injury-induced oxidative stress in rats. Neuroprotective activity was carried out by global cerebral ischemia on Sprague-Dawley rats by bilateral carotid artery (BCA) occlusion for 30 min followed by 60 min reperfusion. The antioxidant enzymatic and non-enzymatic levels were estimated along with cerebral infarction area and histopathological studies. The Matricaria recutita L. methanolic extract showed dose-dependent neuroprotective activity by significant decrease in lipid peroxidation (LPO) and increase in the superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and total thiol levels in extract treated groups as compared to ischemia/reperfusion group. Cerebral infarction area was significantly reduced in extract treated groups as compared to ischemia/reperfusion group. The methanolic extract of Matricaria recutita L. showed potent neuroprotective activity against global cerebral ischemia/reperfusion injury-induced oxidative stress in rats.

Chandrashekhar VM ，Ranpariya VL ，Ganapaty S ，Parashar A ，Muchandi AA ... -  《-》

Evaluation of antioxidant and neuroprotective effect of ethanolic extract of Embelia ribes Burm in focal cerebral ischemia/reperfusion-induced oxidative stress in rats.

Nazam Ansari M ，Bhandari U ，Islam F ，Tripathi CD ... -  《-》

Aged garlic extract delays the appearance of infarct area in a cerebral ischemia model, an effect likely conditioned by the cellular antioxidant systems.

Experimental evidence has shown that some garlic-derived products have a protective effect against ischemic brain injury. The present study was designed to investigate the effect of aged garlic extract (AGE), establish the therapeutic window, and determine its protective mechanism in a cerebral ischemia model. Animals were subjected to middle cerebral artery occlusion (MCAO) for 2h and treated with 1.2ml/kg body wt.(i.p.) of AGE 30min before, at the beginning of (0R), or 1h after reperfusion. The 0R treatment significantly reduced the size of the infarct area after 2h of reperfusion. Repeated doses subsequent to the 0R treatment (at 1, 2, or 3h after reperfusion) had no effect on the temporal window of protection. The protective 0R treatment with AGE prevented the increase in nitrotyrosine and the decrease in total superoxide dismutase, glutathione peroxidase, and extracellular superoxide dismutase activities induced by MCAO. These data indicate that AGE delays the effects of ischemia/reperfusion-induced neuronal injury. However, this treatment itself was not associated with a noticeable improvement in the neurological outcome, or with an effect on the inflammatory response. We conclude that the neuroprotective effect of AGE in the 0R treatment might be associated with control of the free-radical burst induced by reperfusion, preservation of antioxidant enzyme activity, and the delay of other pathophysiological processes.

Aguilera P ，Chánez-Cárdenas ME ，Ortiz-Plata A ，León-Aparicio D ，Barrera D ，Espinoza-Rojo M ，Villeda-Hernández J ，Sánchez-García A ，Maldonado PD ... -  《-》

Protective effect of hydroalcoholic extract of Mimusops elengi Linn. flowers against middle cerebral artery occlusion induced brain injury in rats.

In the traditional Indian and Thai system of medicine, Mimusops elengi Linn., flower is used as brain tonic and to calm anxiety and panic attacks. The present study was designed to investigate the neuroprotective effect of hydroalcoholic extract of Mimusops elengi (ME) against cerebral ischemic reperfusion injury in rats. Male rats were pretreated with ME (100 and 200mg/kg) for seven days and focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) method. After 60min of MCAO and 24h of reperfusion, a battery of behavioral tests assessed the extent of neurological deficits. Infarct volume and brain edema were measured in TTC stained brain sections and the extent of blood brain barrier (BBB) disruption was observed by Evan's blue extravasation. Oxidative and nitrative stress parameters were estimated in the brain homogenates. Further, simultaneous quantification of five polyphenolic biomarkers were done using HPLC. Pretreatment with ME at doses of 100 and 200mg/kg significantly improved the neurobehavioral alterations and reduced the infarct volume, edema and extent of BBB disruption induced by ischemia reperfusion injury. It also prevented the alteration in the antioxidant status and reduced the nitrite levels when compared to ischemic animals. Further, HPLC studies revealed that ME contains five bioactive polyphenolic compounds. These results clearly indicate the neuroprotective effect of ME against stroke like injury. The observed protective effect might be attributed to the polyphenolic compounds and their antioxidant and anti-inflammatory property.

Nagakannan P ，Shivasharan BD ，Thippeswamy BS ，Veerapur VP ，Bansal P ... -  《-》