کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5501158 | 1534626 | 2017 | 63 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Fluctuations in glucose levels induce glial toxicity with glutamatergic, oxidative and inflammatory implications
ترجمه فارسی عنوان
نوسانات سطح گلوکز باعث ایجاد سمیت گلیالیک با اثرات گلوتاماترگیک، اکسیداتیو و التهابی
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کلمات کلیدی
GLUTΔΨmIL-10IL-1βEAAC1GSHNADPHIL-6NFκB - NFKBNOx - NOXp38 MAPK - P38 MAPKROS/RNS - ROS / RNSOxidative/nitrosative stress - استرس اکسید کننده / نیتروژنیکNeuroinflammation - التهاب عصبیNADPH oxidase - اکسیداز NADPH Interleukin 10 - اینترلوکین 10interleukin 1β - اینترلوکین 1βinterleukin 6 - اینترلوکین 6tumor necrosis factor α - تومور نکروز عامل αexcitatory amino acid carrier 1 - حشره شناسی اسید آمینه 1glucose transporters - حمل و نقل گلوکزCNS - دستگاه عصبی مرکزیDiabetes mellitus - دیابت قندیC6 cells - سلولهای C6central nervous system - سیستم عصبی مرکزیTNF-α - فاکتور نکروز توموری آلفاnuclear factor κB - فاکتور هسته ای κBglucose deprivation - محرومیت گلوکزNitric oxide - نیتریک اکسیدnicotinamide adenine dinucleotide phosphate reduced - نیکوتین آمید آدنین دینکلوتید فسفات کاهش می یابدMitochondrial membrane potential - پتانسیل غشای میتوکندریp38 mitogen-activated protein kinase - پروتئین کیناز متیوژن فعال p38Glutathione - گلوتاتیونGlutamine synthetase - گلوتامین سنتتازReactive oxygen/nitrogen species - گونه های واکنشی اکسیژن / نیتروژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
چکیده انگلیسی
Astrocytes are dynamic cells that maintain brain homeostasis by regulating neurotransmitter systems, antioxidant defenses, inflammatory responses and energy metabolism. Astroglial cells are also primarily responsible for the uptake and metabolism of glucose in the brain. Diabetes mellitus (DM) is a pathological condition characterized by hyperglycemia and is associated with several changes in the central nervous system (CNS), including alterations in glial function. Classically, excessive glucose concentrations are used to induce experimental models of astrocyte dysfunction; however, hypoglycemic episodes may also cause several brain injuries. The main focus of the present study was to evaluate how fluctuations in glucose levels induce cytotoxicity. The culture medium of astroglial cells was replaced twice as follows: (1) from 6 mM (control) to 12 mM (high glucose), and (2) from 12 mM to 0 mM (glucose deprivation). Cell viability, mitochondrial function, oxidative/nitrosative stress, glutamate metabolism, inflammatory responses, nuclear factor κB (NFκB) transcriptional activity and p38 mitogen-activated protein kinase (p38 MAPK) levels were assessed. Our in vitro experimental model showed that up and down fluctuations in glucose levels decreased cell proliferation, induced mitochondrial dysfunction, increased oxidative/nitrosative stress with consequent cellular biomolecular damage, impaired glutamate metabolism and increased pro-inflammatory cytokine release. Additionally, activation of the NFκB and p38 signaling pathways were putative mechanisms of the effects of glucose fluctuations on astroglial cells. In summary, for the first time, we show that changes in glucose concentrations, from high-glucose levels to glucose deprivation, exacerbate glial injury.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1863, Issue 1, January 2017, Pages 1-14
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1863, Issue 1, January 2017, Pages 1-14
نویسندگان
André Quincozes-Santos, Larissa Daniele Bobermin, Adriano M. de Assis, Carlos-Alberto Gonçalves, Diogo Onofre Souza,