Protective Effect of Vitamin E in a Rat Model of Focal Cerebral Ischemia

1998 ◽  
Vol 53 (3-4) ◽  
pp. 273-278 ◽  
Author(s):  
M. Stohrer ◽  
Andrea Eichinger ◽  
M. Schlachter ◽  
M. Stangassinger
Keyword(s):  
Vitamin E ◽  
Cerebral Ischemia ◽  
Rat Model ◽  
Oxygen Radicals ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Brain Infarction ◽  
Pathophysiological Mechanism ◽  
Cerebral Ischemia And Reperfusion ◽  
The Right

Abstract Under certain pathological conditions such as cerebral ischemia and reperfusion the occur­rence of free radicals is remarkably increased. However, only very little information is avail­ able on their quantitative relevance for the pathophysiology and final outcome of diseases. The aim of the present study was to evaluate the contribution of oxygen radicals in the pathogenesis of a stroke. For this purpose a rat model for stroke was used. Two of three vitamin E deficient groups were repleted with different dosages of DL-a-tocopherylacetate. N o signs of vitamin E deficiency could be observed. However, the weight gain during reple­tion was increased in the vitamin E repleted groups. Brain infarction was created by occlusion of the right middle cerebral artery (MCAO) for two hours. After 24 hours the measurements of infarct volumes were taken. The infarct volume of the group with the highest repletion dosage was significantly reduced by 81%. This was also expressed in a higher rate of gait disturbances after MCAO of the deficient animals. The control of vitamin E status exhibited a similar repletion-dependent level in plasma and brain. These results strongly support the hypothesis that the generation of oxygen radicals occurring during reperfusion is an impor­tant aspect of the pathophysiological mechanism in brain infarction.

Effect of One Week Treatment with Ginkgo biloba Extract (EGb761) on Ischemia-Induced Infarct Volume in Gerbils

2003 ◽  
Vol 31 (04) ◽  
pp. 533-542 ◽  
Author(s):  
Shu-Ying Chung ◽  
Ming-Fu Wang ◽  
Jing-Ying Lin ◽  
Ming-Cheng Lin ◽  
Hui-Ming Liu ◽  
...  
Keyword(s):  
Locomotor Activity ◽  
Cerebral Ischemia ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Ginkgo Biloba ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Control Group ◽  
Tetrazolium Chloride ◽  
The Right

The present study was designed to evaluate the neuroprotective effects of Ginkgo biloba leaf extract (EGb761) in male gerbils subjected to focal cerebral ischemia produced by permanent occlusion of the right middle cerebral artery. In this study, gerbils were fed standard chow with or without EGb761 (100 mg/kg/day, i.g.) prior to cerebral ischemia for 1 week. Gerbils were anesthetized and craniectomized to expose the right middle cerebral artery (MCA). The right MCA was constricted with an 8-0 suture to produce a permanent ligation. Infarct volume was assessed by TTC (2,3,5-triphenyl-tetrazolium chloride) staining 24 hours after initiation of cerebral ischemia. Results showed that the EGb761 group had significant reduction of infarct volume 4 and 6 mm from the frontal pole by 40% and 30%, respectively when compared to the control group ( p < 0.05). Mean locomotor activity of gerbils was reduced 24 hours after the occlusion of the MCA in both groups. However, there was no difference in locomotor activity between groups either 30 minutes before or 24 hours after the occlusion ( p < 0.05).

Quercetin Protects Against Oxidative Stress Associated Damages in a Rat Model of Transient Focal Cerebral Ischemia and Reperfusion

2011 ◽  
Vol 36 (8) ◽  
pp. 1360-1371 ◽  
Author(s):  
Ajmal Ahmad ◽  
Mohd. Moshahid Khan ◽  
Md. Nasrul Hoda ◽  
Syed Shadab Raza ◽  
M. Badruzzaman Khan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Rat Model ◽  
Focal Cerebral Ischemia ◽  
Ischemia And Reperfusion ◽  
Transient Focal Cerebral Ischemia ◽  
Cerebral Ischemia And Reperfusion

scholarly journals Transplanted Dental Pulp Stem Cells Migrate to Injured Area and Express Neural Markers in a Rat Model of Cerebral Ischemia

2018 ◽  
Vol 45 (1) ◽  
pp. 258-266 ◽  
Author(s):  
Xuemei Zhang ◽  
Yinglian Zhou ◽  
Hulun Li ◽  
Rui Wang ◽  
Dan Yang ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cerebral Ischemia ◽  
Cell Transplantation ◽  
Rat Model ◽  
Dental Pulp ◽  
Therapeutic Potential ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Dental Pulp Stem Cells ◽  
Neural Regeneration

Background/Aims: Ischemic stroke is a major cause of disability and mortality worldwide, while effective restorative treatments are limited at present. Stem cell transplantation holds therapeutic potential for ischemic vascular diseases and may provide an opportunity for neural regeneration. Dental pulp stem cells (DPSCs) origin from neural crest and have neuro-ectodermal features including proliferation and multilineage differentiation potentials. Methods: The rat model of middle cerebral artery occlusion (MCAO) was used to evaluate whether intravenous administration of DPSCs can reduce infarct size and to estimate the migration and trans-differentiation into neuron-like cells in focal cerebral ischemia models. Brain tissues were collected at 4 weeks following cell transplantation and analyzed with immunofluorescence, immunohistochemistry and real-time polymerase chain reaction (RT-PCR) methods. Results: Intravenously administration of rat-derived DPSCs were found to migrate into the boundary of ischemic areas and expressed neural specific markers, reducing infarct volume and cerebral edema. Conclusions: These results suggest that DPSCs treatment may serve as a potential therapy for clinical stroke patients in the future.

scholarly journals Neuroprotective Mechanisms of Calycosin Against Focal Cerebral Ischemia and Reperfusion Injury in Rats

2018 ◽  
Vol 45 (2) ◽  
pp. 537-546 ◽  
Author(s):  
Yong Wang ◽  
Qianyao Ren ◽  
Xing Zhang ◽  
Huiling Lu ◽  
Jian Chen
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Brca1 Gene ◽  
Ischemia And Reperfusion ◽  
Ischemia And Reperfusion Injury ◽  
Neuroprotective Effects ◽  
Cerebral Ischemia And Reperfusion ◽  
Tnf Α

Background/Aims: Emerging evidence suggests that autophagy plays important roles in the pathophysiological processes of cerebral ischemia and reperfusion injury. Calycosin, an isoflavone phytoestrogen, possesses neuroprotective effects in cerebral ischemia and reperfusion in rats. Here, we investigated the neuroprotective effects of calycosin against ischemia and reperfusion injury, as well as related probable mechanisms behind autophagy pathways. Methods: A cerebral ischemic and reperfusion injury model was established by middle cerebral artery occlusion in male Sprague-Dawley rats. Neurological scores, infarct volumes, and brain water content were assessed after 24 h reperfusion following 2 h ischemia. Additionally, the expression of the autophagy-related protein p62 and NBR1 (neighbor of BRCA1 gene 1), as well as Bcl-2, and TNF-α in rat brain tissues was measured by RT-PCR, western blotting and immunohistochemical analyses. Results: The results showed that calycosin pretreatment for 14 days markedly decreased infarct volume and brain edema, and ameliorated neurological scores in rats with focal cerebral ischemia and reperfusion. It was observed that levels of p62, NBR1 and Bcl-2 were greatly decreased, and levels of TNF-α significantly increased after ischemia and reperfusion injury. However, calycosin administration dramatically upregulated the expression of p62, NBR1 and Bcl-2, and downregulated the level of TNF-α. Conclusions: All data reveal that calycosin exerts a neuroprotective effect on cerebral ischemia and reperfusion injury, and the mechanisms maybe associated with its anti-autophagic, anti-apoptotic and anti-inflammatory action.

scholarly journals A Selective N-Type Calcium Channel Antagonist Reduces Extracellular Glutamate Release and Infarct Volume in Focal Cerebral Ischemia

1995 ◽  
Vol 15 (4) ◽  
pp. 611-618 ◽  
Author(s):  
Shunya Takizawa ◽  
Kazushi Matsushima ◽  
Hitoshi Fujita ◽  
Kazunori Nanri ◽  
Saori Ogawa ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Calcium Channel ◽  
Calcium Channel Antagonist ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Glutamate Release ◽  
Extracellular Glutamate ◽  
Neuroprotective Effects ◽  
Significant Difference ◽  
The Right

Although a number of studies have demonstrated the neuroprotective effects of antagonists of postsynaptic N-methyl-d-aspartate (NMDA) and non-NMDA receptors in cerebral ischemia, little is known about the treatment of cerebral infarction through presynaptic blocking of extracellular glutamate release. We evaluated the effects of a presynaptic selective N-type calcium channel antagonist (SNX-111, given intravenously by continuous infusion at 5 mg/kg/h from 20 min prior to occlusion until 2 h postocclusion) on blood flow, extracellular glutamate, and infarct volume in rats with permanent occlusions of the right middle cerebral and right common carotid arteries plus 1-h transient occlusion of the left common carotid artery. There was no significant difference in CBF in the occluded cortex during the experiment between the treated and vehicle groups. SNX-111 significantly reduced total amount of extracellular glutamate during the experiment and the peak value of the glutamate after occlusion from 44.2 ± 15.8 μ M (mean ± SD) to 21.4 ± 11.4 μ M (p < 0.01). Infusion of SNX-111 also significantly reduced the cortical volume of infarction from 47.2 ± 5.8 to 19.9 ± 7.3% (p < 0.0001). These results suggest that SNX-111 has a protective effect against focal ischemia through the inhibition of glutamate release from presynaptic sites, although SNX-111 may also affect the release of other neurotransmitters.

scholarly journals E-Selectin in Focal Cerebral Ischemia and Reperfusion in the Rat

1996 ◽  
Vol 16 (6) ◽  
pp. 1126-1136 ◽  
Author(s):  
Rui Lan Zhang ◽  
Michael Chopp ◽  
Zheng G. Zhang ◽  
M. Laurie Phillips ◽  
Craig L. Rosenbloom ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Cell Damage ◽  
Leukocyte Adhesion ◽  
Infarct Volume ◽  
Ischemia And Reperfusion ◽  
Ischemia And Reperfusion Injury ◽  
Ischemic Lesion ◽  
Mca Occlusion ◽  
Cerebral Ischemia And Reperfusion

The selectin family of glycoproteins facilitates the early phase of polymorphonuclear leukocyte adhesion to the endothelial cell and, thus, may promote ischemic cell damage. To evaluate E-selectin in the pathogenesis of focal cerebral ischemia and reperfusion injury, we cloned rat E-selectin cDNA and measured the temporal profiles E-selectin mRNA (Northern blot) and protein (immunohistochemistry) during (1 h of ischemia) and after (up to 1 week) transient (2 h) middle cerebral artery (MCA) occlusion in the male Wistar rat. We also tested the effect on these rats of administration of CY-1503, an analog of sialyl Lewisx (SLex), on ischemia cell damage. mRNA for E-selectin was first detected in the ischemic hemisphere at 2 h of reperfusion and persisted to 46 h of reperfusion. E-selectin (protein) was localized to microvessels within the ischemic lesion at 0 h of reperfusion and persisted to 70 h of reperfusion. Treatment of the ischemic animals with CY-1503 (50 mg/kg) (n = 8) significantly reduced infarct volume by 42% ( p < 0.05) and significantly reduced myeloperoxidase immunoreactive cells in the ischemic lesion by 60% ( p < 0.05). These findings provide the first direct evidence for the involvement of E-selectin in transient MCA occlusion in rats and suggest that the E-selectin may facilitate neutrophil adhesion and subsequent cerebral ischemic cell damage.

scholarly journals Effects of Pretreatment with a Combination of Melatonin and Electroacupuncture in a Rat Model of Transient Focal Cerebral Ischemia

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Lingguang Liu ◽  
R. T. F. Cheung
Keyword(s):  
Cerebral Ischemia ◽  
Rat Model ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Artery Occlusion ◽  
Sprague Dawley ◽  
Brain Infarct ◽  
Beneficial Effects ◽  
Transient Focal Cerebral Ischemia ◽  
Cerebral Artery Occlusion

Both melatonin and electroacupuncture (EA) have been suggested to be effective treatments against stroke. However, it is unknown whether a combination of these two therapies could be beneficial against transient focal cerebral ischemia. The present study investigated the effects of pretreatment of a combination of melatonin and EA in a rat model of transient middle cerebral artery occlusion (MCAO). After pretreatment of melatonin plus EA (MEA), transient MCAO was induced for 90 minutes in male Sprague-Dawley (SD) rats. The neurological deficit score, brain infarct volume, cerebral edema ratio, neuronal inflammation, and apoptosis were evaluated 24 hours after transient MCAO. The expression of related inflammatory and apoptotic mediators in the brain was also investigated. The results showed that MEA improved neurological outcome, reduced brain infarct volume, and inhibited neuronal inflammation as well as apoptosis 24 hours after transient MCAO. The beneficial effects may derive from downregulation of proinflammatory and proapoptotic mediators and upregulation of antiapoptotic mediators. Thus, these results suggest a preventive effect of pretreatment of MEA on transient focal cerebral ischemia.

scholarly journals Effects of Normobaric Hyperoxia in a Rat Model of Transient Focal Cerebral Ischemia and Reperfusion

Stroke ◽  
2001 ◽  
Vol 32 (suppl_1) ◽  
pp. 316-316
Author(s):  
Aneesh B Singhal ◽  
Xiaoying Wang ◽  
Eng H Lo
Keyword(s):  
Blood Flow ◽  
Cerebral Ischemia ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Blue Dye ◽  
Ischemia And Reperfusion ◽  
Normobaric Hyperoxia ◽  
Doppler Flowmetry ◽  
Normobaric Oxygen ◽  
Cerebral Ischemia And Reperfusion

3 Background: The role of therapeutic oxygen in treatment of acute stroke is controversial. Oxygen improves cellular aerobic metabolism and can salvage ischemic tissue. However, oxygen free radicals can increase blood brain barrier (BBB) damage, and oxygen can induce vasoconstriction, which could worsen stroke outcome. We studied the effects of normobaric oxygen in cerebral ischemia and reperfusion. Methods: Rats were subjected to normobaric hyperoxia (FiO2 100%) or normoxia (FiO2 30%) during two hour filament occlusion and one hour reperfusion of the middle cerebral artery. Twenty-four hour infarct volumes, regional cerebral blood flow (rCBF) using laser Doppler flowmetry, and severity of BBB damage (assessed by quantifying Evan’s Blue dye (EB) leakage after one hour of reperfusion) were compared between groups. Results: Physiological parameters were similar in hyperoxic and control groups, except for paO2, which was expectedly higher in the hyperoxic group (pO2 484 mm Hg) as compared to controls (pO2 118 mm Hg). Mean rCBF dropped to 25% after onset of ischemia and recovered to 75–90% after arterial unocclusion, indicating successful reperfusion. Mean total (right hemispheric) infarct volume was 65 mm 3 in the hyperoxia group and 209 mm 3 in controls, p<0.001. The reduction in infarct volume was mostly in the cortex, where mean infarct volume was 11 mm 3 in hyperoxic rats and 129 mm 3 in controls (p<0.001). Mean striatal infarct volume was 54 mm 3 in hyperoxic rats and 80 mm 3 in controls (p<0.06). Mean total EB leak was 1592 ng/g in hyperoxic and 3955 ng/g in control rats (p<0.02), suggesting reduced BBB damage in hyperoxia. However, BBB damage and EB leak are likely related to infarct volume; after normalising for infarct volume, mean EB leak was 17 ng/mm3 in the hyperoxia group and 14 ng/mm3 in controls (p=0.5). Conclusion: Total and cortical infarct volumes can be significantly reduced with normobaric hyperoxia during transient cerebral ischemia and reperfusion. Hyperoxia does not decrease blood flow to ischemic brain, and its benefit in reducing infarct volume may outweigh any potential damage from BBB damage.

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