کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4337737 | 1614813 | 2014 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Gamma-hydroxybutyrate, acting through an anti-apoptotic mechanism, protects native and amyloid-precursor-protein-transfected neuroblastoma cells against oxidative stress-induced death
ترجمه فارسی عنوان
گاما هیدروکسی بوتیرات، که از طریق مکانیزم ضد آپوپتوتیک عمل می کند، از سلول های نوروبلاستوما بومی و آمیلوئیدی-پروتئین منتقل شده در برابر مرگ ناشی از استرس اکسیداتیو محافظت می کند
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کلمات کلیدی
PBSFACSNADPHDMEMSDSGHBqPCRFITCBSA - BSAMTT - MTTHydrogen peroxide - آب اکسیژنهbovine serum albumin - آلبومین سرم گاوEDTA - اتیلن دی آمین تترا استیک اسید Ethylenediaminetetraacetic acid - اتیلینیدامین تتراستیک اسیدAlzheimer’s disease - بیماری آلزایمرTerminal deoxynucleotidyl transferase-mediated dUTP nick end labeling - ترمینال deoxynucleotidyl transferase-mediated dUTP نام نهایی پایان نامهTUNEL - تونلfluorescence-activated cell sorting - دسته بندی سلول های فعال فلورسنسsodium dodecyl sulfate - سدیم دودسیل سولفاتphycoerythrin - فایکوئیریدینfluorescein isothiocyanate - فلوئورسین ایسوتیوسیاناتNeuroprotection - محافظت نورونی یا محافظت از عصبPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریnicotinamide adenine dinucleotide phosphate - نیکوتین آمید adenine dinucleotide phosphateH2O2 - هیدروژن پراکسیدquantitative polymerase chain reaction - واکنش زنجیره ای پلیمراز کمیoptical density - چگالی نوریGamma-hydroxybutyrate - گاما هیدروکسی بوتیرات
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
چکیده انگلیسی
Clinical observations suggested that gamma-hydroxybutyrate (GHB) protects nerve cells against death but the direct proofs are missing. Here, we combined several approaches to investigate GHB capacity to protect human neuroblastoma SH-SY5Y cells against hydrogen peroxide (H2O2)-induced death. To increase the patho-physiological relevancy of our study, we used native SH-SY5Y cells and SH-SY5Y cells stably transfected with the wild-type amyloid-precursor-protein (APPwt) or control-vector-pCEP4. Trypan Blue exclusion and MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium-bromide) assays combined with pharmacological analyses showed that H2O2 reduced native and genetically modified cell viability and APPwt-transfected cells were the most vulnerable. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) and activated caspase-3 staining assessed by flow cytometry revealed a basally elevated apoptotic signal in APPwt-transfected cells. Reverse-transcription, real-time quantitative polymerase chain reaction (qPCR) and Western blotting showed that mRNA and protein basal ratios of apoptotic modulators Bax/Bcl-2 were also high in APPwt-transfected cells. GHB efficiently and dose-dependently rescued native and genetically modified cells from H2O2-induced death. Interestingly, GHB, which strongly decreased elevated basal levels of TUNEL-staining, activated caspase 3-labeling and Bax/Bcl-2 in APPwt-transfected cells, also counteracted H2O2-evoked increased apoptotic markers in native and genetically modified SH-SY5Y cells. Since GHB did not promote cell proliferation, anti-apoptotic action through the down-regulation of Bax/Bcl-2 ratios and/or caspase 3 activity appears as a critical mechanism involved in GHB-induced protection of SH-SY5Y cells against APPwt-overexpression- or H2O2-evoked death. Altogether, these results, providing multi-parametric evidence for the existence of neuroprotective action of GHB, also open interesting perspectives for the development of GHB analog-based strategies against neurodegeneration or nerve cell death.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 263, 28 March 2014, Pages 203-215
Journal: Neuroscience - Volume 263, 28 March 2014, Pages 203-215
نویسندگان
G. Wendt, V. Kemmel, C. Patte-Mensah, B. Uring-Lambert, A. Eckert, M.J. Schmitt, A.G. Mensah-Nyagan,