کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10836897 | 1066449 | 2005 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Central thyrotropin-releasing hormone increases hepatic cyclic AMP through vagal-cholinergic and prostaglandin-dependent pathways in rats
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کلمات کلیدی
6-OHDAEGTA6-HydroxydopaminePMSFethylene glycol-bis-(2-aminoethylether)-N,N,N′,N′-tetraacetic acidcAMP - cAMPEDTA - اتیلن دی آمین تترا استیک اسید Ethylenediaminetetraacetic acid - اتیلینیدامین تتراستیک اسیدtrh - بازارHepatic regeneration - بازسازی کبدAutonomic nervous system - دستگاه عصبی خودمختار یا خودگردان یا اتونومcentral nervous system - سیستم عصبی مرکزیPhenylmethanesulfonyl fluoride - فنیل متیل سولفونیل فلورایدNeuropeptide - نوروپپتیدthyrotropin-releasing hormone - هورمون آزاد کننده تیروتروپین
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Central thyrotropin-releasing hormone increases hepatic cyclic AMP through vagal-cholinergic and prostaglandin-dependent pathways in rats Central thyrotropin-releasing hormone increases hepatic cyclic AMP through vagal-cholinergic and prostaglandin-dependent pathways in rats](/preview/png/10836897.png)
چکیده انگلیسی
Central neuropeptides play roles in many physiologic regulations through the autonomic nervous system. We have demonstrated that central thyrotropin-releasing hormone (TRH), one of neuropeptides, induces a stimulation of hepatic proliferation through vagal-cholinergic pathways. Since cAMP is known to play an important role in the hepatic proliferation, effect of central TRH on hepatic cAMP was investigated. Rats were intracisternally injected with either a TRH analog, RX-77368 (1-100Â ng), or saline. The liver was removed 2-72Â h after the TRH analog and hepatic cAMP content was determined by radioimmunoassay. In some experiments, pretreatment with hepatic vagotomy, atropine methyl nitrate, or 6-hydroxydopamine (6-OHDA) was performed. Hepatic cAMP was dose-dependently increased by intracisternal TRH analog (5-100Â ng) with a peak response occurring 12Â h postinjection. The central TRH-induced increase in hepatic cAMP was abolished by vagotomy, atropine and indomethacin, but not by 6-OHDA. Intravenous injection of the TRH analog (10Â ng) did not affect hepatic cAMP. These results demonstrate that TRH acts in the brain to increase hepatic cAMP through vagal-cholinergic and prostaglandin-dependent pathways, suggesting that central TRH modulates hepatic functions through cAMP-mediated signaling pathways.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Peptides - Volume 26, Issue 9, September 2005, Pages 1573-1579
Journal: Peptides - Volume 26, Issue 9, September 2005, Pages 1573-1579
نویسندگان
Masashi Yoneda, Toru Kono, Hajime Watanobe, Masaya Tamano, Tadahito Shimada, Hideyuki Hiraishi, Kimihide Nakamura,