Mechanisms of ischemic brain damage

Bhardwaj, Anish; Alkayed, Nabil J.; Kirsch, Jeffrey R.; Hurn, Patricia D.

doi:10.1007/s11886-003-0085-1

Cited by 34 publications

(29 citation statements)

References 71 publications

(71 reference statements)

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“…The signalling pathways of cell death and survival were imbalanced during the cerebral ischemia/reperfusion injury. Over the past decade, many researches have revealed that apoptosis and necrosis are temporally distinct processes of neuronal cell death, which can occur during cerebral ischemia (15). Scientists investigate to fi nd the molecular mechanism of apoptosis and to use this cell death for clinical treatment.…”

Section: Discussionmentioning

confidence: 99%

Assessment of global ischemic/reperfusion and Tacrolimus administration on CA1 region of hippocampus: gene expression profiles of BAX and BCL2 genes

Badr¹,

Hashemi²,

Javadi³

et al. 2016

BLL

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BACKGROUND: It is well known that hippocampus has a pivotal role in learning, formation and consolidation of memory. Global cerebral ischemia causes severe damage to pyramidal neurons of the CA1 region and usually results in residual neurological defi cits following a recovery from ischemia. Scientists investigate to fi nd the molecular mechanism of apoptosis and to use this cell death for clinical treatment. OBJECTIVE: In this investigation, we evaluated the molecular mechanism of FK-506 in apoptosis using gene expression quantifi cation of BAX and BCL-2 genes in hippocampus following global ischemic/reperfusion. MATERIALS AND METHODS: In the present experimental study, adult male Wistar rats were obtained and housed under standard conditions. Each experimental group consisted of fi ve rats and was equally distributed in the normal control, ischemia/reperfusion, ischemia/reperfusion followed by FK-506. Global ischemia was induced for animals in ischemia and drug groups. In the drug group, moreover, two doses of FK-506 were injected as IV injection and intra-peritoneal (IP) injection after 48 h. Then, hippocampus tissue was removed. Consequently, RNA isolated, cDNA was synthesized and Real-Time PCR was performed. Finally, the obtained data was analyzed statistically (p < 0.05). RESULTS: The quantitative results showed the BAX expression ratio increased approximately 3-times in ischemia/reperfusion (3.11 ± 0.28) group compared to the untreated (NR) and the drug group (p < 0.001). The statistical analysis showed a signifi cant difference for BCL-2 expression between the experimental groups (p<0.001). The mRNA level of BCL-2 decreased in the ischemia/reperfusion group, while it was without alteration in the other groups. CONCLUSION: The results showed that global cerebral ischemia/reperfusion induced BAX as pro-apoptotic gene and tacrolimus a neuroprotective drug inhibited BAX gene expression and induced BCL-2 gene expression as anti-apoptotic gene (Tab. 2, Fig. 3, Ref. 21). Text in PDF www.elis.sk.

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Section: Discussionmentioning

confidence: 99%

Assessment of global ischemic/reperfusion and Tacrolimus administration on CA1 region of hippocampus: gene expression profiles of BAX and BCL2 genes

Badr¹,

Hashemi²,

Javadi³

et al. 2016

BLL

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“…Depending on the amount and production origin, NO can have favorable or damaging effects in ischemic brain [29]. Endothelial and inducible nitric oxide synthase (iNOS) have been implicated in protection induced by ischemic preconditioning in brain [30,31].…”

Section: Nitric Oxide (No)mentioning

confidence: 99%

Inhalational anesthetics as preconditioning agents in ischemic brain

Wang

Traystman

Murphy

2008

Current Opinion in Pharmacology

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“…Though reperfusion restores cerebral blood flow, it may induce secondary brain injury and cerebral edema [20]. In this study, we measured the BWC 24 h after reperfusion and found that it was increased compared to the Sham, suggesting that the rats with GCIR had cerebral edema.…”

Section: Translational Neurosciencementioning

confidence: 64%

Protective effect of tea polyphenols on the blood-brain barrier

Xue

Gao

et al. 2013

Translational Neuroscience

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This study was to investigate the protective effects of tea polyphenols on the blood-brain barrier (BBB) of rats with global cerebral ischemia/reperfusion (GCIR) injury. Sprague Dawley rats underwent four-vessel occlusion to construct the model of GCIR. Half an hour before complete occlusion, they were treated with tea polyphenols (TP) (6.4%; 100 or 200 mg/kg) via tail intravenous injection. 24 h after reperfusion, BBB permeability was evaluated by measuring brain water content (BWC) and residual amount of Evan's blue dye in cerebral tissue. In addition to this, MMP-9 and collagen IV protein expression in cerebral tissue were also detected using immunohistochemistry. ANOVA and SNK-q were used to do statistical analysis. Statistical significance was considered at P<0.05. Compared to the untreated, the TP-treated rats had significantly decreased BWC (P<0.05), decreased residual amount of Evan's blue dye in cerebral tissue (P<0.05), down-regulated MMP-9 (P<0.05) and up-regulated collagen IV expression in brain tissue (P<0.05). It can be concluded from these findings that TP may reduce the MMP-9 mediated collagen IV degradation caused by GCIR to protect the BBB.

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Mechanisms of ischemic brain damage

Cited by 34 publications

References 71 publications

Assessment of global ischemic/reperfusion and Tacrolimus administration on CA1 region of hippocampus: gene expression profiles of BAX and BCL2 genes

Assessment of global ischemic/reperfusion and Tacrolimus administration on CA1 region of hippocampus: gene expression profiles of BAX and BCL2 genes

Inhalational anesthetics as preconditioning agents in ischemic brain

Protective effect of tea polyphenols on the blood-brain barrier

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