کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5846299 | 1128474 | 2014 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Analysis of changes in hepatic gene expression in a murine model of tolerance to acetaminophen hepatotoxicity (autoprotection)
ترجمه فارسی عنوان
تجزیه و تحلیل تغییرات در بیان ژن کبدی در یک مدل موشهای تحمل به سمیت قلبی استامینوفن (حفاظت خودکار)
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کلمات کلیدی
APAPMMLV-RTH202MAT1AFMO3VNN1LGALS3MRPPPARi.p.CCl4CFBqRT-PCRALTHydrogen peroxide - آب اکسیژنهgene array - آرایه ژنAlanine aminotransferase - آلانین آمینوترانسفرازAcetaminophen - استامینوفن intraperitoneal - داخل صفاقیHepatotoxicity - سمیت کبدnuclear factor (erythroid-derived 2)-like 2 - فاکتور هسته ای (erythroid-derived 2) -like 2flavin-containing monooxygenase 3 - مونواکسینژاز 3 حاوی فلاوینwild type - نوع وحشیquantitative real-time polymerase chain reaction - واکنش زنجیره ای پلیمراز کمی زمان واقعی استmoloney murine leukemia virus reverse transcriptase - ویروس لوکسی مولینای لوکمی ویروسی معکوسmultidrug resistance-associated protein - پروتئین مرتبط با مقاومت چند داروییLiver - کبدCarbon tetrachloride - کربن تتراکلریدclofibrate - کلافیبرتGalectin-3 - گالکتین-3Peroxisome proliferator activated receptor - گیرنده فعال فعال پروکسیوم
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
چکیده انگلیسی
Pretreatment of mice with a low hepatotoxic dose of acetaminophen (APAP) results in resistance to a subsequent, higher dose of APAP. This mouse model, termed APAP autoprotection was used here to identify differentially expressed genes and cellular pathways that could contribute to this development of resistance to hepatotoxicity. Male C57BL/6J mice were pretreated with APAP (400Â mg/kg) and then challenged 48Â h later with 600Â mg APAP/kg. Livers were obtained 4 or 24Â h later and total hepatic RNA was isolated and hybridized to Affymetrix Mouse Genome MU430_2 GeneChip. Statistically significant genes were determined and gene expression changes were also interrogated using the Causal Reasoning Engine (CRE). Extensive literature review narrowed our focus to methionine adenosyl transferase-1 alpha (MAT1A), nuclear factor (erythroid-derived 2)-like 2 (Nrf2), flavin-containing monooxygenase 3 (Fmo3) and galectin-3 (Lgals3). Down-regulation of MAT1A could lead to decreases in S-adenosylmethionine (SAMe), which is known to protect against APAP toxicity. Nrf2 activation is expected to play a role in protective adaptation. Up-regulation of Lgals3, one of the genes supporting the Nrf2 hypothesis, can lead to suppression of apoptosis and reduced mitochondrial dysfunction. Fmo3 induction suggests the involvement of an enzyme not known to metabolize APAP in the development of tolerance to APAP toxicity. Subsequent quantitative RT-PCR and immunochemical analysis confirmed the differential expression of some of these genes in the APAP autoprotection model. In conclusion, our genomics strategy identified cellular pathways that might further explain the molecular basis for APAP autoprotection.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology and Applied Pharmacology - Volume 274, Issue 1, 1 January 2014, Pages 156-167
Journal: Toxicology and Applied Pharmacology - Volume 274, Issue 1, 1 January 2014, Pages 156-167
نویسندگان
Meeghan A. O'Connor, Petra Koza-Taylor, Sarah N. Campion, Lauren M. Aleksunes, Xinsheng Gu, Ahmed E. Enayetallah, Michael P. Lawton, José E. Manautou,