کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6273439 | 1614801 | 2014 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Aging causes exacerbated ischemic brain injury and failure of sevoflurane post-conditioning: Role of B-cell lymphoma-2
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کلمات کلیدی
STAT3tPAMCAOBcl-2ECLTTCMAPK - MAPKmiddle cerebral artery occlusion - انسداد شریان (سرخرگ) مغزی میانیBax - باکسenhanced chemiluminescence - بهبود شیمیایی لومنApoptosis - خزان یاختهایAging - سالخوردگیIschemic stroke - سکته مغزی ایسکمیکtissue plasminogen activator - فعال کننده بافتی پلاسمینوژنB-cell lymphoma-2 - لنفوم سلول B-2Signal transducer and activator of transcription-3 - مبدل سیگنال و فعال کننده رونویسی 3Bcl-2-associated X protein - پروتئین X مرتبط با Bcl-2mitogen-activated protein kinase - پروتئین کیناز فعال با mitogen
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Aging is associated with exacerbated brain injury after ischemic stroke. Herein, we explored the possible mechanisms underlying the age-associated exacerbated brain injury after ischemic stroke and determined whether therapeutic intervention with anesthetic post-conditioning would provide neuroprotection in aged rats. Male Fisher 344 rats (young, 4Â months; aged, 24Â months) underwent 2Â h of middle cerebral artery occlusion (MCAO) followed by 24-h reperfusion, with or without sevoflurane post-conditioning for 15Â min immediately at the onset of reperfusion. Compared with young rats, aged rats showed larger infarct size, worse neurological scores and more TUNEL-positive cells in the penumbral cerebral cortex at 24Â h after MCAO. However, edema formation and motor coordination were similar in both groups. Sevoflurane reduced the infarct size, edema formation, and TUNEL-positive cells, and improved the neurological outcome in young rats but not in aged rats. Molecular studies revealed that basal expression of the anti-apoptotic molecule B-cell lymphoma-2 (Bcl-2) in the brain was lower in aged rats compared with young rats before MCAO, while basal expression of the pro-apoptotic molecule Bcl-2-associated X protein (Bax) showed similar levels in both groups. MCAO reduced Bcl-2 expression and increased Bax expression in both groups; however, Bax increase was more pronounced in aged rats. In young rats, sevoflurane reversed the above MCAO-induced changes. In contrast, sevoflurane failed to enhance Bcl-2 expression but decreased Bax expression in aged rats. These findings suggest that aging-associated reduction in basal Bcl-2 expression in the brain contributes to increased neuronal injury by enhancing cell apoptosis after ischemic stroke. Sevoflurane post-conditioning failed to provide neuroprotection in aged rats, probably due to its inability to increase Bcl-2 levels and prevent apoptosis in the brain.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 275, 5 September 2014, Pages 2-11
Journal: Neuroscience - Volume 275, 5 September 2014, Pages 2-11
نویسندگان
P. Dong, J. Zhao, Y. Zhang, J. Dong, L. Zhang, D. Li, L. Li, X. Zhang, B. Yang, W. Lei,