کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10739120 | 1046862 | 2005 | 16 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Cinnamophilin reduces oxidative damage and protects against transient focal cerebral ischemia in mice
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کلمات کلیدی
HPCDCINNPBSMCA4-HNE4-hydroxynonenallCBFLDFRNS8-OHdG8-hydroxy-2′-deoxyguanosine - 8-هیدروکسی-2'-دگزسی گوانوزینHET - ITROS - ROSOxidative damage - آسیب اکسیداتیوFocal cerebral ischemia - ایسکمی مغز مرکزی کانونیSuperoxide - سوپر اکسیدStroke - سکته مغزیmiddle cerebral artery - شریان مغزی میانیlaser-Doppler flowmetry - فلومتر لیزر داپلرNeuroprotection - محافظت نورونی یا محافظت از عصبPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریHydroethidine - هیدروتیدینHydroxypropyl-β-cyclodextrin - هیدروکسی پروپیل بتا-سیکلوکودکسترینreactive nitrogen species - گونه های واکنش پذیر نیتروژنReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Acute neuroprotective effects of cinnamophilin (CINN; (8R, 8â²S)-4, 4â²-dihydroxy-3, 3â²-dimethoxy-7-oxo-8, 8â²-neolignan), a novel antioxidant and free radical scavenger, were studied in a mouse model of transient middle cerebral artery (MCA) occlusion. CINN was administered intraperitoneally either 15 min before (pretreatment) or 2 h after the onset of MCA occlusion (postischemic treatment). Relative to vehicle-treated controls, animals pretreated with CINN, at 20-80 mg/kg, had significant reductions in brain infarction by 33-46% and improvements in neurobehavioral outcome. Postischemic administration with CINN (80 mg/kg) also significantly reduced brain infarction by 43% and ameliorated neurobehavioral deficits. Additionally, CINN administration significantly attenuated in situ accumulation of superoxide anions (O2â) in the boundary zones of infarct at 4 h after reperfusion. Consequently, CINN-treated animals exhibited significantly decreased levels of oxidative damage, as assessed by immunopositive reactions for 8-hydroxy-2â²-deoxyguanosine (8-OHdG) and 4-hydroxynonenal (4-HNE), and the resultant inflammatory reactions at 24 h postinsult. It is concluded that CINN effectively reduced brain infarction and improved neurobehavioral outcome following a short-term recovery period after severe transient focal cerebral ischemia in mice. The finding of a decreased extent of reactive oxygen species and oxidative damage observed with CINN treatment highlights that its antioxidant and radical scavenging ability is contributory.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 39, Issue 4, 15 August 2005, Pages 495-510
Journal: Free Radical Biology and Medicine - Volume 39, Issue 4, 15 August 2005, Pages 495-510
نویسندگان
E.-Jian Lee, Hung-Yi Chen, Ming-Yang Lee, Tsung-Ying Chen, Yun-Shang Hsu, Yu-Ling Hu, Guan-Liang Chang, Tian-Shung Wu,