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Başlık: Peripheral GLP-1 gastroprotection against ethanol: The role of exendin, NO, CGRP, prostaglandins and blood flow
Yazarlar: Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Anabilim Dalı.
0000-0003-0863-1547
İşbil, Naciye Büyükcoşkun
Güleç, Güldal
Çam, Betül Etöz
Özlük, Kasım
C-5730-2015
AAH-1692-2021
55665951400
6602752303
24179406800
6602676331
Anahtar kelimeler: CGRP-(8-37)
Exendin-(9-39)
Gastric mucosal blood flow
Gastric mucosal damage
Glucagon like peptide-1
Indomethacin
l-NAME
Glucagon-like peptide-1
Gene-related peptide
Gastric somatostatin
Experimental-models
Rat
Receptor
Lesions
Amylin
Amide
Mechanisms
Endocrinology & metabolism
Physiology
Rattus
Yayın Tarihi: 8-Oca-2009
Yayıncı: Elsevier
Atıf: İşbil, N. B. vd. (2009). "Peripheral GLP-1 gastroprotection against ethanol: The role of exendin, NO, CGRP, prostaglandins and blood flow". Regulatory Peptides, 152(1-3), 22-27.
Özet: The aim of this study was to investigate the effects of peripherally injected glucagon like peptide-1 (GLP-1) on ethanol-induced gastric mucosal damage and the mechanisms included in the effect. Absolute ethanol was administered through an orogastric cannula right after the injection of GLP-1 (1, 10, 100, 1000 or 10,000 ng/kg; i.p.). The rats were decapitated an hour later, the stomachs removed and the gastric mucosal damage scored. 1000 ng GLP-1 inhibited gastric mucosal damage by 45% and 10,000 ng GLP-1 by 60%. The specific receptor antagonist exendin-(9-39) (2500 ng/kg; i.p.), calcitonin gene related peptide (CGRP) receptor antagonist CGRP-(8-37) (10 pg/kg; i.p.), nitric oxide (NO) synthase inhibitor L-NAME (30 mg/kg; s.c) and cyclooxygenase inhibitor indomethacin (5 mg/kg; i.p.) inhibited the preventive effect of GLP-1 on ethanol-induced gastric mucosal damage. GLP-1 also prevented the decrease in gastric mucosal blood flow caused by ethanol when administered at gastroprotective doses (1000 and 10,000 ng/kg: i.p.). In conclusion, GLP-1 administered peripherally prevents the gastric mucosal damage caused by ethanol in rats. CGRR NO, prostaglandin and gastric mucosal blood flow are thought to play a role in this effect, mediated through receptors specific to GLP-1.
URI: https://doi.org/10.1016/j.regpep.2008.09.006
https://www.sciencedirect.com/science/article/pii/S016701150800164X
http://hdl.handle.net/11452/24138
ISSN: 0167-0115
Koleksiyonlarda Görünür:Scopus
Web of Science

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