کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9000624 | 1116548 | 2005 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Nitrofurazone-induced gene expressions in rat hepatocytes and their modification by N-acetylcysteine
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کلمات کلیدی
c-fosCyclin D1Cyclin ETransforming growth factor-α (TGF-α)c-Ha-ras - c-ha-rasc-Myc - c-mycN-acetylcysteine - N-استیل سیستئینGene expression - بیان ژنProliferation - ترویجc-Jun - جون ژوئنEpidermal growth factor (EGF) - عامل رشد اپیدرمال (EGF)Hepatocyte growth factor (HGF) - عامل رشد هپاتوسیت (HGF)Tumor necrosis factor-α (TNF-α) - عامل نکروز تومور-α (TNF-α)Rat - موش صحراییNitrofurazone - نیترو فورازونHepatocyte - هپاتوسیت
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم کشاورزی و بیولوژیک
علوم دامی و جانورشناسی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Nitrofurazone-induced gene expressions in rat hepatocytes and their modification by N-acetylcysteine Nitrofurazone-induced gene expressions in rat hepatocytes and their modification by N-acetylcysteine](/preview/png/9000624.png)
چکیده انگلیسی
The antibiotic nitrofurazone (NF) at a subtoxic dose has been shown to increase hepatocyte DNA synthesis with no preceding cell damage or necrosis. This was suppressed by concomitant administration of the antioxidant N-acetylcysteine (NAC), which suggests that free radical production is involved in the process. In this study, male F344 rats were given a single oral subtoxic dose of NF to investigate the changes in genes implicated in hepatocyte proliferation between 1 and 20 h postdose by real-time PCR. Some rats were also given NAC to examine the involvement of free radicals. There were transient and sequential increases in mRNA levels of c-myc and c-jun shortly after the administration, followed by tumor necrosis factor-α (TNF-α), transforming growth factor-α (TGF-α), c-Ha-ras, and cyclin E. The increases were blocked by concomitant administration of NAC. In contrast, there were no NF-specific increases in c-fos, hepatocyte growth factor, epidermal growth factor or cyclin D1 mRNAs. These results indicate that the induction of hepatocyte proliferation by NF is triggered by free radicals, with a pathway involving increases in c-jun, c-myc, TNF-α, TGF-α, c-Ha-ras, and cyclin E. The results also indicate that NF-induced proliferation resembles that of other mitogens.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental and Toxicologic Pathology - Volume 56, Issue 6, 29 April 2005, Pages 333-339
Journal: Experimental and Toxicologic Pathology - Volume 56, Issue 6, 29 April 2005, Pages 333-339
نویسندگان
Kyoko Ito, Satoru Kajikawa, Aisuke Nii, Kunio Doi,