کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6274614 | 1614830 | 2013 | 31 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Propofol prevents cerebral ischemia-triggered autophagy activation and cell death in the rat hippocampus through the NF-κB/p53 signaling pathway
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کلمات کلیدی
PFT-α3-MATBSTLC3PaCO2PaO2GAPDHDRAMp53-upregulated modulator of apoptosisPifithrin-alphaNF-κBdamage-regulated autophagy modulatorPBSp533-methyladenine - 3-متیل آدنینBSA - BSADMSO - DMSOI/R - I / RSDS–PAGE - SDS-PAGEbovine serum albumin - آلبومین سرم گاوAutophagy - اتوفاژیsodium dodecyl sulfate–polyacrylamide gel electrophoresis - الکتروفورز ژل دوده سولفات سدیم پلی آکریل آمیدstandard deviation - انحراف معیارCerebral ischemia - ایسکمی مغزیischemia–reperfusion - ایسکمی-رپرفیوژنanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of varianceDimethylsulfoxide - دیمتیل سولفواکسیدH/I - سلامNuclear factor-kappa B - فاکتور هسته ای-کاپا BPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریhypoxia–ischemia - هیپوکسی-ایسکمیpolymerase chain reaction - واکنش زنجیره ای پلیمرازPCR - واکنش زنجیرهٔ پلیمرازmicrotubule-associated protein 1 light chain 3 - پروتئین مرتبط با میکروتوبول 1 زنجیره سبک 3Propofol - پروپوفولPUMA - پوماglyceraldehyde-3-phosphate dehydrogenase - گلیسرالیدید-3-فسفات دهیدروژناز
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Propofol (2,6-diisopropylphenol) has been shown to attenuate neuronal injury under a number of experimental conditions; however, the mechanisms involved in its neuroprotective effects remain unclear. We therefore investigated whether inhibition of p53 induction by propofol contributes to the neuroprotection of cerebral ischemic cell death through both autophagic and apoptotic mechanisms. A transient global cerebral ischemia-reperfusion (I/R) model was produced with a 10-min, 2-vessel occlusion. The change in target genes including damage-regulated autophagy modulator (DRAM), microtubule-associated protein 1 light chain 3 (LC3), Beclin 1, cathepsin D, cathepsin B, p53-upregulated modulator of apoptosis (PUMA), Bax and Bcl-2 upon p53 inhibition was assessed with the co-administration of the intravenous anesthetic propofol and 3-methyladenine (3-MA), Pifithrin-alpha (PFT-α) or SN50. The I/R-induced increases of protein levels of p53 and LC3-II were significantly inhibited by treatment with propofol, 3-MA or PFT-α. The I/R-induced increases of protein levels of DRAM, Beclin 1, active cathepsin D and cathepsin B were significantly inhibited by treatment with propofol, PFT-α or SN50. The negative effects of the I/R-induced up-regulation of PUMA and Bax and the down-regulation of Bcl-2 in the rat hippocampus were all blocked by treatment with propofol, PFT-α or SN50. Our results suggest that cerebral I/R can induce nuclear factor-kappa B-dependent expression of p53. The autophagic and apoptotic mechanisms participate in programed cell death by regulating the p53-mediated pathway. Our results are the first to show that propofol, at clinically relevant concentrations, attenuated cell death through both autophagic and apoptotic mechanisms in the rat hippocampus after a cerebral I/R insult.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 246, 29 August 2013, Pages 117-132
Journal: Neuroscience - Volume 246, 29 August 2013, Pages 117-132
نویسندگان
D.R. Cui, L. Wang, W. Jiang, A.H. Qi, Q.H. Zhou, X.L. Zhang,