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Chinese Journal of Applied Physiology ; (6): 136-140, 2015.
Article in Chinese | WPRIM | ID: wpr-243399

ABSTRACT

<p><b>OBJECTIVE</b>To explore the effect of 3-n-butylphthalide pretreatment on the delayed neuronal death(DND) and the expreesion of heat shock protein70 (HSP70) in rat hippocampus after ischemia/ reperfusion.</p><p><b>METHODS</b>All rats were randomly divided into sham group (n = 36), total cerebral ischemia (TCI) group (n = 36), butylphthalide (NBP) group (n = 6), NBP + TCI group( n = 36), quercetin + NBP + TCI group (n = 6), dimethyl sulfoxide (DMSO) + NBP + TCI group (n = 6). The model of total cerebral ischemia/reperfusion was established by blocking vertebral arteries and carotid arteries. In sham group, TCI group and NBP group, the animals were further divided into instantly, 6 h, 12 h, 1 d, 3 d, 5 d groups according to the time interval after sham operation or TCI. Histological changes of the hippocampus were evaluated using thionin staining under light microscope by determining the delayed neuronal death (DND) and the expression of HSP70 was assayed using immunohistochemistry.</p><p><b>RESULTS</b>NBP pretreatment could reduce delayed neuronal death in CA1 of hippocampus induced by TCI-reperfusion injury in rats, and up-regulated the expression of HSP70 in CA1 hippocampus of brain ischemic/reperfusion for 5 days. Quercetin blocked the acquirement of the brain ischemic tolerance induced by NBP preconditioning.</p><p><b>CONCLUSION</b>3-n-butylphthalide (NBP) prevents the neurons from ischemia/reperfusion injury through upregulating the expression of HSP70.</p>


Subject(s)
Animals , Rats , Benzofurans , Pharmacology , CA1 Region, Hippocampal , Cell Biology , Pathology , Cell Death , Cerebral Infarction , Drug Therapy , HSP70 Heat-Shock Proteins , Metabolism , Ischemic Preconditioning , Neurons , Cell Biology , Rats, Wistar , Reperfusion Injury , Drug Therapy
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