Cerebral ischemia model with conscious mice

Himori, Noriko; Watanabe, Hiroshi; Akaike, Nobuhide; Kurasawa, Mitsue; Itoh, Jiro; Tanaka, Yushiro

doi:10.1016/0160-5402(90)90059-t

Cited by 71 publications

(6 citation statements)

References 27 publications

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“…The noted neuronal injury (increase in infarct size & motor incoordination) induced by global cerebral ischemia/reperfusion is in line with our earlier reports [21,26] and reports from other laboratories [28,29]. …”

Section: Discussionsupporting

confidence: 93%

Effect of Neurosteroid Modulation on Global Ischaemia-Reperfusion-Induced Cerebral Injury in Mice

Grewal

Jaggi

Rana

et al. 2013

Korean J Physiol Pharmacol

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The present study was designed to investigate the putative effect of neurosteroid modulation on global ischaemia-reperfusion-induced cerebral injury in mice. Bilateral carotid artery occlusion followed by reperfusion, produced a significant rise in cerebral infarct size along with impairment of grip strength and motor coordination in Swiss albino mice. Administration of carbamazepine (16 mg/kg, i.p.) before global cerebral ischaemia significantly attenuated cerebral infarct size and improved the motor performance. However, administration of indomethacin (100 mg/kg, i.p.) attenuated the neuroprotective effect of carbamazepine. Mexiletine (50 mg/kg, i.p.) did not produce significant neuroprotective effect. It may be concluded that the neuroprotective effect of carbamazepine may be due to increase in synthesis of neurosteroids perhaps by activating enzyme (3α HSD) as indomethacin attenuated the neuroprotective effect of carbamazepine. The sodium channel blocking effect of carbamazepine may not be involved in neuroprotection as mexiletine, a sodium channel blocker, did not produce significant neuroprotective effect.

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Section: Discussionsupporting

confidence: 93%

Effect of Neurosteroid Modulation on Global Ischaemia-Reperfusion-Induced Cerebral Injury in Mice

Grewal

Jaggi

Rana

et al. 2013

Korean J Physiol Pharmacol

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“…Global cerebral ischemia was induced surgically according to methods of Himori et al ., (1990)[ 11 ] and as described by Kaur et al ., (2010). [ 6 ] Mice were anesthetized using chloral hydrate (400 mg/kg, ip ).…”

Section: Methodsmentioning

confidence: 99%

Pharmacological evidence for connection of nitric oxide-mediated pathways in neuroprotective mechanism of ischemic postconditioning in mice

Gulati

Singh

2014

J Pharm Bioall Sci

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Introduction:Postconditioning (PoCo) is an adaptive phenomenon whereby brief repetitive cycles of ischemia with intermittent reperfusion instituted immediately after prolonged ischemia at the onset of prolonged reperfusion elicit tissue protection. PoCo is noted to exert a protective effect in various organs like heart, liver, kidney and brain. Various triggers, mediators and end effectors are suggested to contribute to the protective effect of PoCo. However, the neuroprotective mechanism of PoCo is poorly understood.Objectives:The present study has been designed to investigate the role of nitric oxide pathway in the neuroprotective mechanism of ischemic postconditioning (iPoCo) employing a mouse model of global cerebral ischemia and reperfusion-induced injury.Materials and Methods:Bilateral carotid artery occlusion (BCAO) of 12 min followed by reperfusion for 24 h was employed to produce ischemia and reperfusion (I/R)-induced cerebral injury in mice. Cerebral injury was assessed in the terms of cerebral infarct, memory impairment and motor in-coordination. Brain nitrite/nitrate; acetylcholinesterase activity, thiobarbituric acid reactive species (TBARS) and glutathione level were also estimated.Results:BCAO followed by reperfusion produced a significant rise in cerebral infarct size, memory impairment and motor incoordination. Further a rise in acetylcholinesterase activity and TBARS level along with fall in brain nitrite/nitrate and glutathione levels was also noted. iPoCo consisting of three episodes of 10 s carotid artery occlusion and reperfusion (instituted immediately after BCAO) significantly attenuated infarct size, memory impairment, motor incoordination as well as altered biochemicals. iPoCo-induced neuroprotective effects were significantly abolished by pretreatment of L-NAME, a nonselective NOS inhibitor.Conclusion:It may be concluded that the nitric oxide pathway probably plays a vital role in the neuroprotective mechanism of iPoCo.

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“…Pulling the ends of the thread with constant weight induced global cerebral ischemia. After 15 min of global cerebral ischemia, the weight on the thread was removed to allow reflow of blood through carotid arteries and the incision was sutured back in layers [32]. Temperature was maintained at 37°C throughout the surgical procedure.…”

Section: Methodsmentioning

confidence: 99%

Evaluation of Antioxidant and Cerebroprotective Effect of Medicago sativa Linn. against Ischemia and Reperfusion Insult

Bora¹,

Sharma

2011

Evidence-Based Complementary and Alternative Medicine

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Antioxidants have been the focus of studies for developing neuroprotective agents to be used in the therapy for stroke, which is an acute and progressive neurodegenerative disorder. Medicago sativa (MS) has a long tradition of use as ayurvedic and homoeopathic medicine in central nervous system disorders. The plant has been reported to have antioxidant, anti-inflammatory and antidiabetic effects. Therefore, the present study was designed to investigate the neuroprotective effect of methanol extract of MS on ischemia and reperfusion-induced cerebral injury in mice. Bilateral carotid artery occlusion (BCAO) for 15 min followed by 24-h reperfusion, resulted in significant elevation in infarct size, xanthine oxidase (XO) activity, superoxide anion (O•− 2) production and thiobarbituric acid-reactive substance (TBARS) levels, and significant depletion in endogenous antioxidant [reduced glutathione (GSH), superoxide dismutase (SOD) and total tissue sulfhydryl (T-SH) groups] systems in mice brain. Further, BCAO led to impairment in short-term memory and motor coordination. Pre-treatment with MS (100 or 200 mg kg−1, p.o.) markedly reduced cerebral infarct size, XO, O•− 2 and TBARS levels, significantly restored GSH, SOD and T-SH levels and attenuated impairment in short-term memory and motor coordination. In addition, MS directly scavenged free radicals generated against a stable radical 1,1-diphenyl-2-picrylhydrazyl and O•− 2 generated in phenazine methosulphate-nicotinamide adenine dinucleotide systems, and also inhibited XD/XO conversion and resultant O•− 2 production. The data from this study suggest that treatment with MS enhances the antioxidant defense against BCAO-induced global cerebral ischemia and exhibits neuroprotective activity.

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Cerebral ischemia model with conscious mice

Cited by 71 publications

References 27 publications

Effect of Neurosteroid Modulation on Global Ischaemia-Reperfusion-Induced Cerebral Injury in Mice

Effect of Neurosteroid Modulation on Global Ischaemia-Reperfusion-Induced Cerebral Injury in Mice

Pharmacological evidence for connection of nitric oxide-mediated pathways in neuroprotective mechanism of ischemic postconditioning in mice

Evaluation of Antioxidant and Cerebroprotective Effect of Medicago sativa Linn. against Ischemia and Reperfusion Insult

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