کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8553384 | 1562586 | 2018 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Course-, dose-, and stage-dependent toxic effects of prenatal dexamethasone exposure on fetal articular cartilage development
ترجمه فارسی عنوان
اثرات سمی، دوره ای، دوز و مرحله ای از قرار گرفتن در معرض دگزامتازون پیش از تولد در رشد غضروف مفصلی جنین
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کلمات کلیدی
Sox9prenatal dexamethasone exposureSRY-box 9IUGRsingle exposureTGFβR1Col2a1MODIODPDERT-qPCRTGFβTransforming Growth Factor Beta - تبدیل بتا فاکتور رشدTransforming growth factor β - تبدیل فاکتور رشد βintegrated optical density - تراکم نوری یکپارچهDexamethasone - دگزامتازونgestational day - روز بارداریDevelopmental toxicity - سمیت توسعهRepeated exposure - قرار گرفتن در معرضPrenatal exposure - قرار گرفتن در معرض پیش از قاعدگیintrauterine growth restriction - محدودیت رشد داخل رحمیmean optical density - میانگین تراکم نوریreal-time quantitative polymerase chain reaction - واکنش زنجیره ای پلیمراز کمی زمان واقعی است
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
چکیده انگلیسی
Dexamethasone, a synthetic long-acting glucocorticoid, is routinely used for treating mothers at risk for preterm delivery. However, intrauterine overexposure to glucocorticoids induces low birth weight and cartilage dysplasia in offspring. Also, the “critical window” and safe dose of this treatment are largely unknown. This study investigated the course-, dose-, and stage-dependent toxic effects and the possible mechanisms of prenatal dexamethasone exposure (PDE) on fetal development and articular cartilage development. Pregnant mice (C57BL/6) received subcutaneous injection of dexamethasone (0.8â¯mg/kgâ¯d) once on gestational day (GD) 15 or once a day from GD 15 to 17, or received various doses of dexamethasone (0, 0.2, 0.8, and 1.2â¯mg/kgâ¯d) on GD 15-17, or received dexamethasone (0.8â¯mg/kgâ¯d) at early stage (GD 12-14) or late stage of pregnancy (GD 15-17). Offspring's knee joints were harvested at birth for morphological analyses and detection of gene expression. Repeated PDE significantly suppressed fetal and articular cartilage development, which were characterized by decreased body weight and body length, coarse articular cartilage surfaces, and reduced gene and protein expression of Col2a1 and aggrecan. For those newborns treated with repeated PDE at different doses, the toxic effects on fetal and articular cartilage development were observed at doses of 0.8 and 1.2â¯mg/kgâ¯d, whereas no obvious toxic effects were observed at the dose of 0.2â¯mg/kgâ¯d. Moreover, PDE at 0.8â¯mg/kgâ¯d during the early embryonic stage induced stronger toxic effects on fetal and articular cartilage development, compared with PDE during the late embryonic stage. Detection of gene expression showed that the TGFβ signaling pathway in the articular cartilage was down-regulated after PDE. Taken together, PDE induces fetal developmental toxicity and articular cartilage developmental toxicity in a course-, dose-, and stage-dependent manner.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology Letters - Volume 286, April 2018, Pages 1-9
Journal: Toxicology Letters - Volume 286, April 2018, Pages 1-9
نویسندگان
Ze Chen, Zhe Zhao, Yunzepeng Li, Xingyu Zhang, Bin Li, Liaobin Chen, Hui Wang,