کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9416053 | 1614329 | 2005 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Diazoxide preconditioning attenuates global cerebral ischemia-induced blood-brain barrier permeability
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
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چکیده انگلیسی
Brain edema formation due to blood-brain barrier (BBB) disruption is a major consequence of cerebral ischemia. Previously, we demonstrated that targeting mitochondrial ATP-sensitive potassium channels (mitoKATP) protects neuronal tissues in vivo and in vitro, however, the effects of mitoKATP openers on cerebral endothelial cells and on BBB functions have never been examined. We investigated the effects of mitoKATP channel opener diazoxide on BBB functions during ischemia/reperfusion injury (I/R). Rats were treated with 6, 20 or 40 mg/kg diazoxide ip for 3 days then exposed to global cerebral ischemia for 30 min. BBB permeability was assessed by administering Evan's-blue (EB) and Na-fluorescein (NaF) at the beginning of the 30 min reperfusion. I/R increased BBB permeability for the large molecular weight EB (ng/mg) in the cortex (control: 146 ± 12, n = 7; I/R: 1049 ± 152, n = 11) which was significantly attenuated in diazoxide-treated rats (575 ± 99, n = 9; 582 ± 104, n = 8; 20 and 40 mg/kg doses). Diazoxide pretreatment also significantly inhibited the extravasation of the low molecular weight NaF. Edema formation in the cortex was also decreased after diazoxide pretreatment. In cultured cerebral endothelial cells, diazoxide depolarized the mitochondrial membrane, suggesting a direct diazoxide effect on the endothelial mitochondria. Our results demonstrate that preconditioning of cerebral endothelium with diazoxide protects the BBB against ischemic stress.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1051, Issues 1â2, 27 July 2005, Pages 72-80
Journal: Brain Research - Volume 1051, Issues 1â2, 27 July 2005, Pages 72-80
نویسندگان
Gábor Lenzsér, Béla Kis, Ferenc Bari, David W. Busija,