کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9426590 | 1295927 | 2005 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Post-ischemic delivery of the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor rosuvastatin protects against focal cerebral ischemia in mice via inhibition of extracellular-regulated kinase-1/-2
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کلمات کلیدی
eNOSHMG-CoALDFECLiNOSERKTBSJnkMCA3-hydroxy-3-methylglutaryl coenzyme A - 3 هیدروکسی 3-متیل گلوتاریل کوآنزیم Ainducible NO synthase - NO سنتاز القاء شدهStatin - استاتینendothelial NO synthase - اندوتلیال NO سنتازTris-buffered saline - تریس بافر شورlaser Doppler flow - جریان داپلر لیزرmiddle cerebral artery - شریان مغزی میانیNeuroprotection - محافظت نورونی یا محافظت از عصبmap - نقشهSignal transduction - هدایت سیگنالmitogen-activated protein - پروتئین فعال mitogenenhanced chemoluminescence - چمولومینسانس پیشرفتهJun kinase - ژوئن کینازextracellular-regulated kinase - کیناز تنظیم شده خارج سلولی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
After recent clinical trials, statins have gained increasing significance in secondary stroke prevention. From experimental studies, it is well established that statins have beneficial action when delivered prophylactically prior to a stroke. Conversely, much less is known about the effects of statins on injury development when delivered after ischemia. We here examined the effects of a post-ischemic delivery of rosuvastatin (0.5, 5 or 20mg/kg, administered i.p. immediately after reperfusion onset), a potent 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, on brain injury and cell signaling after focal cerebral ischemia, induced by 90 min of intraluminal middle cerebral artery occlusion in mice. In animals receiving normal saline, 0.5 or 5mg/kg rosuvastatin, middle cerebral artery occlusions resulted in reproducible brain infarcts at 24 h after reperfusion onset, which did not differ in size. However, rosuvastatin, administered at higher doses (20mg/kg), reduced infarct volume at 24 and 48 h after ischemia (by 34±16% and 18±3%, respectively, P<0.05). Western blots revealed that rosuvastatin decreased phosphorylated extracellular-regulated kinase-1/-2 and reduced activated caspase-3 levels in ischemic brain areas, while endothelial NO synthase expression, p38 and Jun kinase phosphorylation were not influenced by the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor. Rosuvastatin also significantly diminished expression levels of inducible NO synthase in the ischemic brain. Our results indicate that rosuvastatin may have utility not only as stroke prophylaxis but also as acute therapy inhibiting executive cell death pathways.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 134, Issue 3, 2005, Pages 901-906
Journal: Neuroscience - Volume 134, Issue 3, 2005, Pages 901-906
نویسندگان
Ã. Kilic, C.L. Bassetti, E. Kilic, H. Xing, Z. Wang, D.M. Hermann,