کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
11033458 | 1613743 | 2018 | 18 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Time dependent neuroprotection of dexamethasone in experimental focal cerebral ischemia: The involvement of NF-κB pathways
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
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چکیده انگلیسی
We propose that the neuroprotective effect of glucocorticoid in ischemic damage may be time dependent. The present study was designed to test the proposal and its possible mechanism in cerebral ischemia/reperfusion (I/R) injury model. Reperfusion injury was induced after 120â¯min of middle cerebral artery occlusion (MCAO) in male Sprague-Dawley rats. At different time points after MCAO, rats were treated with high dose dexamethasone (10â¯mg/kg), and neurological deficit and infarct sizes were measured 2â¯h, 24â¯h after MCAO. The expression of NF-κB target genes, including inducible nitric oxide synthase (iNOS), cyclooxygenase (COX-2), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), were determined by western blot analysis and ELISA. Dexamethasone delivered 30â¯min (but not 60â¯min, 120â¯min) after MCAO markedly decreased the infarct size, improved neurological deficits in I/R injury model. Dexamethasone delivered 30â¯min (but not 60â¯min) after MCAO significantly inhibited NF-κB p65 expression and phosphorylation, compared with I/R group. The expression of iNOS, COX-2, TNF-α and IL-1β, were also suppressed by dexamethasone delivered 30â¯min (but not 60â¯min) after MCAO. The results imply that neuroprotective action of dexamethasone in focal ischemic stroke model may be time dependent and attributed to inhibiting inflammation-related NF-κB p65 pathways.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1701, 15 December 2018, Pages 237-245
Journal: Brain Research - Volume 1701, 15 December 2018, Pages 237-245
نویسندگان
Wen-Hao Sun, Fan He, Nan-Nan Zhang, Zi-Ai Zhao, Hui-Sheng Chen,