Urotensin receptors as a new target for CLP induced septic lung injury in mice
 
Yazarlar (7)
Prof. Dr. Elif Çadırcı Atatürk Üniversitesi, Türkiye
Rüstem Anıl Ugan Atatürk Üniversitesi, Türkiye
Doç. Dr. Büşra Dincer Atatürk Üniversitesi, Türkiye
Doç. Dr. Betül Gündoğdu Atatürk Üniversitesi, Türkiye
Doç. Dr. İrfan ÇINAR Kastamonu Üniversitesi, Türkiye
Erol Akpınar Atatürk Üniversitesi, Türkiye
Prof. Dr. Zekai Halıcı Atatürk Üniversitesi, Türkiye
Makale Türü Özgün Makale (SSCI, AHCI, SCI, SCI-Exp dergilerinde yayınlanan tam makale)
Dergi Adı Naunyn Schmiedeberg S Archives of Pharmacology (Q3)
Dergi ISSN 0028-1298 Wos Dergi Scopus Dergi
Dergi Tarandığı Indeksler SCI-Expanded
Makale Dili İngilizce Basım Tarihi 02-2019
Cilt / Sayı / Sayfa 392 / 2 / 135–145 DOI 10.1007/s00210-018-1571-8
Makale Linki http://dx.doi.org/10.1007/s00210-018-1571-8
Özet
Sepsis is a life-threatening organ dysfunction condition response resulting in acute lung injury. Urotensin II (UII), an endogenous vasoactive peptide, is widely distributed in pulmonary, cardiovascular, central nervous, renal and metabolic systems, and especially in inflammatory regions. This study aimed to investigate whether urotensin II (UII) and UII receptor (UTR) antagonists play a role in the inflammatory response to sepsis-induced lung damage and they are possible therapeutic targets. In the study, 78 male Balb-c mice were used. A cecal ligation and puncture (CLP)-induced polymicrobial sepsis model was applied, and the effects of human urotensin II (agonist) and urantide and palosuran (antagonists) were investigated on lung tissues. Glutathione and malondialdehyde levels and SOD activity of lung tissues were investigated in addition to TNF-α, IL-1β, IL-6, NF-κB, and UTR mRNA levels. Also, lung sections …
Anahtar Kelimeler
Lung damage | Palosuran | Sepsis | Urantide | Urotensin | Urotensin receptor
BM Sürdürülebilir Kalkınma Amaçları
Atıf Sayıları
Web of Science 38
Scopus 39
Google Scholar 53
Urotensin receptors as a new target for CLP induced septic lung injury in mice

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