کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8479269 | 1551309 | 2014 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Role of hydrogen sulfide in secondary neuronal injury
ترجمه فارسی عنوان
نقش سولفید هیدروژن در آسیب های عصبی ثانویه
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کلمات کلیدی
NeuromodulatorIL-1βIP3NMDAN-methyl-d-aspartatePLCPKCIAPSGluTsHcyAOAAPLPCBSNaHSp38MAPKPPGHSP 90γ-GCS1-methyl-4-phenylpyridinium ionTBISUR2Bd,l-PropargylglycineMACOalpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acidAMPApKaMCP-1H2SCSESAMcAMP - cAMPcystathionine γ-lyase - cystationine γ-lyaseERK1/2 - ERK1 / 2MPP+ - MPP +NF-кB - NF-kBROS - ROSS-adenosyl methionine - S-آدنوزیل متیونینγ-glutamylcysteine synthetase - γ-گلوتامیل سستئین سینتاتازCyclic adenosine monophosphate - آدنوزین مونوفسفات Cyclicadenylate cyclase - آدنیلات سیکلاسTraumatic brain injury - آسیب تروماتیک مغزSpinal cord injury - آسیب نخاعیAminooxyacetate - آمینوسیسی سکتهInterleukin-1β - اینترلوکین-1βAlzheimer’s disease - بیماری آلزایمرlong term potentiation - تقویت طولانی مدتLTP - تقویت طولانی مدت یا LTP tumor necrosis factor-α - تومور نکروز عامل αglutamate transporters - حمل و نقل گلوتاماتCNS - دستگاه عصبی مرکزیHydrogen sulfide - سولفید هیدروژنcystathionine β-synthase - سیستاتیونین β-سنتازcentral nervous system - سیستم عصبی مرکزیsci - علمیTNF-α - فاکتور نکروز توموری آلفاnuclear factor kappa B - فاکتور هسته ای کاپا Bphospholipase C - فسفولیپاز CMechanism - مکانیسم یا سازوکارRole - نقشNitric oxide - نیتریک اکسیدhomocysteine - هوموسیستئینSodium hydrosulfide - هیدرو سولفید سدیمHydroxylamine - هیدروکسیلامینMonocyte chemotactic protein-1 - پروتئین chemotactic monocyte-1Heat shock protein 90 - پروتئین شوک حرارت 90protein kinase A - پروتئین کیناز AProtein kinase C - پروتئین کیناز سیp38 mitogen activated protein kinase - پروتئین کیناز فعال میتوکندر P38pyridoxal 5′-phosphate - پیریدوکسال 5'-فسفاتKATP channels - کانال های KATPReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
چکیده انگلیسی
In acute neuronal insult events, such as stroke, traumatic brain injury, and spinal cord injury, pathological processes of secondary neuronal injury play a key role in the severity of insult and clinical prognosis. Along with nitric oxide (NO) and carbon monoxide (CO), hydrogen sulfide (H2S) is regarded as the third gasotransmitter and endogenous neuromodulator and plays multiple roles in the central nervous system under physiological and pathological states, especially in secondary neuronal injury. The endogenous level of H2S in the brain is significantly higher than that in peripheral tissues, and is mainly formed by cystathionine β-synthase (CBS) in astrocytes and released in response to neuronal excitation. The mechanism of secondary neuronal injury exacerbating the damage caused by the initial insult includes microcirculation failure, glutamate-mediated excitotoxicity, oxidative stress, inflammatory responses, neuronal apoptosis and calcium overload. H2S dilates cerebral vessels by activating smooth muscle cell plasma membrane ATP-sensitive K channels (KATP channels). This modification occurs on specific cysteine residues of the KATP channel proteins which are S-sulfhydrated. H2S counteracts glutamate-mediated excitotoxicity by inducing astrocytes to intake more glutamate from the extracellular space and thus increasing glutathione in neurons. In addition, H2S protects neurons from secondary neuronal injury by functioning as an anti-oxidant, anti-inflammatory and anti-apoptotic mediator. However, there are still some reports suggest that H2S elevates neuronal Ca2+ concentration and may contribute to the formation of calcium overload in secondary neuronal injury. H2S also elicits calcium waves in primary cultures of astrocytes and may mediate signals between neurons and glia. Consequently, further exploration of the molecular mechanisms of H2S in secondary neuronal injury will provide important insights into its potential therapeutic uses for the treatment of acute neuronal insult events.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurochemistry International - Volume 64, January 2014, Pages 37-47
Journal: Neurochemistry International - Volume 64, January 2014, Pages 37-47
نویسندگان
Jun-Feng Wang, Yu Li, Jin-Ning Song, Hong-Gang Pang,