کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5859273 | 1562337 | 2014 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Involvement of miRNAs in the early phase of halothane-induced liver injury
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کلمات کلیدی
RORγtMIP-2CyPAPAPCXCL1GAPDHALTMAPK - MAPKβ-actin - β-اکتینcycle threshold - آستانه چرخهDrug-induced liver injury - آسیب کبدی ناشی از مواد مخدرAlanine aminotransferase - آلانین آمینوترانسفرازAcetaminophen - استامینوفن ISO - ایزوIsoflurane - ایزوفلوران interleukin - اینترلوکینDILI - دیلیCytochrome P450 - سیتوکروم پی۴۵۰Actb - عملMicroRNA - میکرو RNA MiRNA - میکروRNA، ریزآرانای، miRNAHalothane - هالوتانmacrophage inflammatory protein 2 - پروتئین التهابی ماکروفاژ 2mitogen-activated protein kinase - پروتئین کیناز فعال با mitogenHal - چیزchemokine (C-X-C motif) ligand 1 - کیموکین (C-X-C motif) لیگاند 1
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Involvement of miRNAs in the early phase of halothane-induced liver injury Involvement of miRNAs in the early phase of halothane-induced liver injury](/preview/png/5859273.png)
چکیده انگلیسی
MicroRNAs (miRNA) form a class of small non-coding RNA molecules that negatively regulate gene expression. Most cellular pathways are modulated by miRNAs. However, the pathophysiological role of miRNAs during drug-induced liver injury (DILI) remains largely unknown. In this study, the possible involvement of miRNAs in DILI caused by the hepatotoxic drug halothane (HAL) was investigated. Toward this purpose, miRNA microarray studies of HAL-induced liver injury were performed in mice at five different time points up to 24Â h after dosing. To exclude any pharmacological effects on miRNA expression, isoflurane was used as a low hepatotoxic drug because it is structurally similar to HAL. Approximately 30-50% of the miRNA expression levels changed more than two-fold at every time point. In silico biological pathway analysis was performed to predict the targeted genes. Consequently, the miRNA gene down-regulation that occurred 1Â h after HAL administration was primarily related to inflammation, immune systems and liver injury. Based on additional in silico analyses, we identified miR-106b. Subsequently target of miR-106b was investigated using liver samples from mice with HAL-induced liver injury. Among the predicted targets, we discovered that a signal transducer and activator of transcription 3 (STAT3) was particularly up-regulated beginning during the early phase of HAL-induced liver injury. Collectively, the suppressed miR-106b expression, as well as the subsequent up-regulation of STAT3, was critical for the pathogenesis of HAL-induced liver injury.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology - Volume 319, 7 May 2014, Pages 75-84
Journal: Toxicology - Volume 319, 7 May 2014, Pages 75-84
نویسندگان
Shinya Endo, Azusa Yano, Tatsuki Fukami, Miki Nakajima, Tsuyoshi Yokoi,