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Search Results: 1 - 10 of 4855 matches for " focal cerebral ischemia/reperfusion "
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Synthesis and Protective Effect of Scutellarein on Focal Cerebral Ischemia/Reperfusion in Rats
Lihua Qian,Minzhe Shen,Hao Tang,Yuping Tang,Li Zhang,Yifan Fu,Qianping Shi,Nian-Guang Li
Molecules , 2012, DOI: 10.3390/molecules170910667
Abstract: Scutellarein, the main metabolite of scutellarin in vivo, has relatively better solubility, bioavailability and bio-activity than scutellarin. However, compared with scutellarin, it is very difficult to obtain scutellarein from Nature. Therefore, the present study focused on establishing an efficient route for the synthesis of scutellarein by hydrolyzing scutellarin. Neurological deficit score and cerebral infarction volume with the administration of scutellarein were then used to compare its neuroprotective effects on focal cerebral ischemia/reperfusion in rats induced by middle cerebral artery occlusion (MCAO) with those of scutellarin. The results showed that scutellarein had better protective effect on focal cerebral ischemia/reperfusion than scutellarin, which laid the foundation for further research and development of scutellarein as a promising candidate for ischemic cerebro-vascular disease.
Aminoguanidine reduces infarct volume and improves neurological dysfunction in transient model of focal cerebral ischemia in rat
Abedin Vakili,Aliakbarar Nekooeian,Gholam Abbas Dehghani
DARU : Journal of Pharmaceutical Sciences , 2006,
Abstract: Focal cerebral ischemia (Stroke) is the cessation or severe reduction of blood flow to an area of the brain that through activation of a complex cytotoxic cascade results in neuronal cell death. The present study was designed to examine the effects of post-ischemic treatment with aminoguanidine (AG) on cortical, striatal infarct volume as well as neurological dysfunctions. Rats (n=23) were allocated to sham, saline or AG (300 mg/kg)-treated groups. Ischemia was induced by 90 minutes middle cerebral artery occlusion, followed by 24 hrs reperfusion. Saline or AG was administered intraperitoneal at one hour after induction of ischemia. At the end of 24hrs reperfusion, neurological deficit score was tested and cortical, striatal infarct volumes were determined by Triphenyltetrazolium chloride staining. Administration of AG (300 mg/kg) at one hours after ischemia resulted in a significantly lower cortical (85±25 vs. 210±13 mm3), striatal (35±5 vs. 58±10 mm3) infarct volumes, and neurological deficit score (1.88±0.23 vs. 2.67±0.21). Our findings indicate that aminoguanidine is a potent neuroprotective in rat model of transient focal cerebral ischemia. The future studies are required to clear cerebroprotective mechanism of aminoguanidine and possible use of this agent as a therapeutic target in stroke patients.
Functional evaluation of temporary focal cerebral ischemia: experimental model
Duarte, Sinésio Grace;Campos, Ant?nio Dorival;Colli, Benedicto Oscar;
Arquivos de Neuro-Psiquiatria , 2003, DOI: 10.1590/S0004-282X2003000500009
Abstract: objective: despite cerebral ischemia being a frequent clinical pathologic state, the tolerance of neural tissue to oxygen absence and to reperfusion is controversial. this study aims to evaluate the effects of focal cerebral ischemia/reperfusion, by analyzing the mitochondrial respiration. method: sixty-four adult rats underwent focal cerebral ischemia by middle cerebral artery occlusion, during 15, 30 and 60 minutes, followed by 10 minutes or 19 hours of reperfusion. the effects of ischemia were analyzed measuring the o2 consumption by mitochondria in the ischemic and non-ischemic areas. results: there was compromise of the mitochondrial respiration after 30 and 60 minutes of ischemia, followed by 10 minutes of reperfusion but there was no alteration in this function after 19 hours of reperfusion. conclusion: compromise of the mitochondrial function occurred after 30 minutes of ischemia but, until one hour of ischemia, if the reperfusion was prolonged there was no evidence of ischemic/reperfusion injuries.
Functional evaluation of temporary focal cerebral ischemia: experimental model
Duarte Sinésio Grace,Campos Ant?nio Dorival,Colli Benedicto Oscar
Arquivos de Neuro-Psiquiatria , 2003,
Abstract: OBJECTIVE: Despite cerebral ischemia being a frequent clinical pathologic state, the tolerance of neural tissue to oxygen absence and to reperfusion is controversial. This study aims to evaluate the effects of focal cerebral ischemia/reperfusion, by analyzing the mitochondrial respiration. METHOD: Sixty-four adult rats underwent focal cerebral ischemia by middle cerebral artery occlusion, during 15, 30 and 60 minutes, followed by 10 minutes or 19 hours of reperfusion. The effects of ischemia were analyzed measuring the O2 consumption by mitochondria in the ischemic and non-ischemic areas. RESULTS: There was compromise of the mitochondrial respiration after 30 and 60 minutes of ischemia, followed by 10 minutes of reperfusion but there was no alteration in this function after 19 hours of reperfusion. CONCLUSION: Compromise of the mitochondrial function occurred after 30 minutes of ischemia but, until one hour of ischemia, if the reperfusion was prolonged there was no evidence of ischemic/reperfusion injuries.
Neuroprotective effect of mild hypothermia in the temporary brain ischemia in cats
Nakano, Hiroshi;Colli, Benedicto Oscar;Lopes, Luiza da Silva;
Arquivos de Neuro-Psiquiatria , 2007, DOI: 10.1590/S0004-282X2007000500015
Abstract: objective: to evaluate the neuroprotective effect of mild hypothermia during temporary focal ischemia in cats. method: 20 cats underwent middle cerebral artery 60 minutes occlusion and 24 hours reperfusion: 10 under normothermia and 10 under mild hypothermia (32o c). brain coronal sections 2mm thick were stained with 2,3,5-triphenyltetrazolium hydrochloride, photographed and evaluated with software for volume calculation. results:cortical ischemia was found in 7 and basal ganglia ischemia in 8 animals of group 1 and in both regions in 5 animals of group 2 (no difference: p=0.6499 for cortical; p=0.3498 for basal ganglia). no ischemia was found in 5 animals of group 2 and in none of group 1 (significant difference, p=0.0325). the infarct volume was greater in group 1 than 2 (p=0.0433). conclusion: mild hypothermia did not interfere with location of ischemia, but it was effective for reducing the infarct volume.
Effect of dimethyl sulfoxide on injuries and neurological deficits: a rat model of transient focal cerebral ischemia
Vakili A
Tehran University Medical Journal , 2008,
Abstract: "nBackground: Dimethyl sulfoxide (DMSO) has been used as a solvent for many drugs in ischemic experiments. DMSO has many biological benefits, including antioxidant, anti-inflammatory, platelet aggregation inhibiting and cell membrane stabilizing effects. Moreover, some experimental studies report that DMSO has a neurprotective effect in permanent focal cerebral ischemia. Despite the effect of DMSO on the cortex, striatum injuries and motor neurological dysfunctions in transient focal cerebral ischemia are not completely clear. "nMethods: Thirty-six male Sprague-Dawley rats weighing 300-350 g were divided into saline- (control) and DMSO-treated groups. Under chloral hydrate anesthesia (400mg/kg, ip), transient focal cerebral ischemia was induced by 90-min middle cerebral artery occlusion (MCAO) followed by 23-h reperfusion. Rats received saline (n=11) or 2% DMSO intraperitoneally at doses of 0.01 (n=11), 0.1 (n=7) and 0.2 (n=7) ml/kg 30 min prior to induction of ischemia. Twenty-four hours after MCAO, the neurological deficit scores were ascertained. Cortical and striatal infarct volumes determined by triphenyltetra-zolium chloride staining. "nResults: Administration of DMSO at doses of 0.1 and 0.2 ml/kg significantly reduced cortical and striatal infarct volumes (p<0.001), while rats receiving the 0.1 ml/kg dose had infarct volumes similar to those of the control group (p=0.225). Moreover, only 0.2 ml/kg doses of DMSO significantly reduce neurological motor dysfunction (p<0.001). "nConclusions: Findings of this study indicate that DMSO is a potent neuroprotective agent against transient focal cerebral ischemia in rat. Moreover, our data also suggest that DMSO may be a candidate for acute stroke treatment.
Evaluation the protective effect of aminoguanidine on cortex and striatum damage in acute phase of focal cerebral ischemia in rat
Abedin Vakili,Toctam Sadough,Mahdi Zahedikhorasani
Physiology and Pharmacology , 2007,
Abstract: Introduction: Several studies have indicated that late treatment of aminoguanidine (AG) reduces cerebral ischemic injuries in animal models. However, the effects of early treatment of AG on cerebral ischemic damage are not well understood. This study was designed to evaluate effect of early treatment of AG on cortex and striatum injuries as well as neurological dysfunctions in transient model of focal cerebral ischemia. Methods: Rats (n=30) were assigned to control or AG treated groups (75 or 150 mg/kg, i.p.,). Ischemia was induced by 60 min middle cerebral artery occlusion, followed by 24h reperfusion. Saline (control) or AG were administered at the onset of the ischemia. Twenty-four hours after the end of ischemia, neurological dysfunction scores were determined and then the infarct volumes of cortex and striatum were measured. Results: Administration of AG (75 and 150 mg/kg) at the beginning of ischemia, significantly reduced cortical and striatal infarct volumes by 47%, 69% and 42%, 36%, respectively (p<0.001). Moreover, AG only at dose 150 mg/kg significantly improves neurological dysfunction (p<0.01). Conclusion: Results of this study indicated that administration of AG in early phase of focal cerebral ischemia reduced cortical and striatal infarct volumes and improve neurological deficits in rat model of transient focal cerebral ischemia.
Effect of policosanol on cerebral ischemia in Mongolian gerbils
Molina, V.;Arruzazabala, M.L.;Carbajal, D.;Valdés, S.;Noa, M.;Más, R.;Fraga, V.;Menéndez, R.;
Brazilian Journal of Medical and Biological Research , 1999, DOI: 10.1590/S0100-879X1999001000014
Abstract: policosanol is a mixture of higher aliphatic primary alcohols isolated from sugar cane wax, whose main component is octacosanol. an inhibitory effect of policosanol on platelet aggregation and cerebral ischemia in animal models has been reported. thus, the objective of the present study was to evaluate the effect of policosanol on cerebral ischemia induced by unilateral carotid ligation and bilateral clamping and recirculation in mongolian gerbils. policosanol (200 mg/kg) administered immediately after unilateral carotid ligation and at 12- or 24-h intervals for 48 h significantly inhibited mortality and clinical symptoms when compared with controls, whereas lower doses (100 mg/kg) were not effective. control animals showed swelling (tissue vacuolization) and necrosis of neurons in all areas of the brain studied (frontal cortex, hippocampus, striatum and olfactory tubercle), showing a similar injury profile. in the group treated with 200 mg/kg policosanol swelling and necrosis were significantly reduced when compared with the control group. in another experimental model, comparison between groups showed that the brain water content of control gerbils (n = 15) was significantly higher after 15 min of clamping and 4 h of recirculation than in sham-operated animals (n = 13), whereas policosanol (200 mg/kg) (n = 19) significantly reduced the edema compared with the control group, with a cerebral water content identical to that of the sham-operated animals. camp levels in the brain of control-ligated mongolian gerbils (n = 8) were significantly lower than those of sham-operated animals (n = 10). the policosanol-treated group (n = 10) showed significantly higher camp levels (2.68 pmol/g of tissue) than the positive control (1.91 pmol/g of tissue) and similar to those of non-ligated gerbils (2.97 pmol/g of tissue). in conclusion, our results show an anti-ischemic effect of policosanol administered after induction of cerebral ischemia, in two different experimental models i
Effect of policosanol on cerebral ischemia in Mongolian gerbils
Molina V.,Arruzazabala M.L.,Carbajal D.,Valdés S.
Brazilian Journal of Medical and Biological Research , 1999,
Abstract: Policosanol is a mixture of higher aliphatic primary alcohols isolated from sugar cane wax, whose main component is octacosanol. An inhibitory effect of policosanol on platelet aggregation and cerebral ischemia in animal models has been reported. Thus, the objective of the present study was to evaluate the effect of policosanol on cerebral ischemia induced by unilateral carotid ligation and bilateral clamping and recirculation in Mongolian gerbils. Policosanol (200 mg/kg) administered immediately after unilateral carotid ligation and at 12- or 24-h intervals for 48 h significantly inhibited mortality and clinical symptoms when compared with controls, whereas lower doses (100 mg/kg) were not effective. Control animals showed swelling (tissue vacuolization) and necrosis of neurons in all areas of the brain studied (frontal cortex, hippocampus, striatum and olfactory tubercle), showing a similar injury profile. In the group treated with 200 mg/kg policosanol swelling and necrosis were significantly reduced when compared with the control group. In another experimental model, comparison between groups showed that the brain water content of control gerbils (N = 15) was significantly higher after 15 min of clamping and 4 h of recirculation than in sham-operated animals (N = 13), whereas policosanol (200 mg/kg) (N = 19) significantly reduced the edema compared with the control group, with a cerebral water content identical to that of the sham-operated animals. cAMP levels in the brain of control-ligated Mongolian gerbils (N = 8) were significantly lower than those of sham-operated animals (N = 10). The policosanol-treated group (N = 10) showed significantly higher cAMP levels (2.68 pmol/g of tissue) than the positive control (1.91 pmol/g of tissue) and similar to those of non-ligated gerbils (2.97 pmol/g of tissue). In conclusion, our results show an anti-ischemic effect of policosanol administered after induction of cerebral ischemia, in two different experimental models in Mongolian gerbils, suggesting a possible therapeutic effect in cerebral vascular disorders.
Effects of delayed estrogen treatment and 20-HETE synthesis inhibition on postischemic pial artery response to acetylcholine in rats  [PDF]
Chikao Miyazaki, Emil N. Zeynalov, Raymond C. Koehler, Marguerite T. Littleton-Kearney
Open Journal of Molecular and Integrative Physiology (OJMIP) , 2014, DOI: 10.4236/ojmip.2014.41001
Abstract:

Relatively little is known about the effects of estrogen on postischemic cerebral vasomotor dynamics after ischemic injury. Emerging hypotheses suggest that the timing after menopause at which hormone replacement is initiated might be important and might modulate the potential benefits of estrogen on brain rescue once a cerebral ischemic event occurs. Therefore, we sought to determine if protracted hypoestrogenicity modifies estrogen’s protective effects on postischemic pial artery dilatory dysfunction and if the arachidonic acid metabolite 20-hydroxyeicosatetraeonic (20-HETE) contributes to the dysfunction. Pial artery dilation to acetylcholine was examined before and 1 hour after 15 minutes forebrain ischemia. The rat study groups included: sexually mature males (M), naive (N), OVX (OV), estrogen-treated OVX females (E1; estrogen started 1 week post ovariectomy) and delayed estrogen-treated (E10; started 10 weeks post ovariectomy) females. Postischemic responses were assessed before and after superfusion of the 20-HETE synthesis inhibitor N-hydroxy-N’-(4-butyl-2-methylphenyl)-formamidine (HET0016). Postischemic acetylcholine dilation was depressed in M, OV and E10 compared to N and E1 rats. Compared to E1, delayed estrogen replacement worsened acetylcholine-induced dilation. Postischemic microvascular estrogen receptor alpha (ERα) density was similar in the OV, E1 and E10 rats. Postischemic application of HET0016 failed to improve acetylcholine dilation. Continuous infusion of HET0016 during and after ischemia did not reverse postischemic pial vasodilatory dysfunction. Timing of estrogen replacement may be critical for vascular health after cerebral ischemic injury. Postischemic loss of acetylcholine reactivity does not appear to involve mechanisms related to 20-HETE synthesis or microvascular ERα expression.

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