Liang-Ming Liu1, Liang Zhao1, Dong-Yu Liang1, Fang-Ping Yu1, Chang-Gen Ye1, Wen-Juan Tu1, Tong Zhu1. 1. Liang-Ming Liu, Liang Zhao, Dong-Yu Liang, Fang-Ping Yu, Chang-Gen Ye, Wen-Juan Tu, Tong Zhu, Department of Hepatology, Songjiang Hospital Affiliated to the First People's Hospital, Shanghai Jiaotong University, Shanghai 201600, China.
Abstract
AIM: To investigate urotensin-II (UII) and its effects on tumor necrosis factor (TNF)-α and interleukin (IL)-1β in early acute liver failure (ALF). METHODS: We investigated the time-dependent alteration in UII levels and its effects on TNF-α and IL-1β in liver and blood in the early stage of lipopolysaccharide/D-galactosamine-induced ALF. RESULTS: After lipopolysaccharide/D-galactosamine challenge, UII rose very rapidly and reached a maximal level 0.5 h, and the level remained significantly elevated after 2 h (P < 0.05). Six hours after challenge, UII began to degrade, but remained higher than at 0 h (P < 0.05). Pretreatment with urantide, an inhibitor of the UII receptor, suppressed the degree of UII increase in liver and blood at 6 h after challenge (P < 0.05 vs paired controls). In addition, liver and blood TNF-α increased from 1 to 6 h, and reached a peak at 1 and 2 h, respectively; however, IL-1β did not rise until 6 h after challenge. Urantide pretreatment inhibited the degree of TNF-α and IL-1β increase following downregulation of UII post-challenge (all P < 0.05). CONCLUSION: UII plays a role in the pathogenesis and priming of ALF by triggering an inflammatory cascade and driving the early release of cytokines in mice.
AIM: To investigate urotensin-II (UII) and its effects on tumor necrosis factor (TNF)-α and interleukin (IL)-1β in early acute liver failure (ALF). METHODS: We investigated the time-dependent alteration in UII levels and its effects on TNF-α and IL-1β in liver and blood in the early stage of lipopolysaccharide/D-galactosamine-induced ALF. RESULTS: After lipopolysaccharide/D-galactosamine challenge, UII rose very rapidly and reached a maximal level 0.5 h, and the level remained significantly elevated after 2 h (P < 0.05). Six hours after challenge, UII began to degrade, but remained higher than at 0 h (P < 0.05). Pretreatment with urantide, an inhibitor of the UII receptor, suppressed the degree of UII increase in liver and blood at 6 h after challenge (P < 0.05 vs paired controls). In addition, liver and blood TNF-α increased from 1 to 6 h, and reached a peak at 1 and 2 h, respectively; however, IL-1β did not rise until 6 h after challenge. Urantide pretreatment inhibited the degree of TNF-α and IL-1β increase following downregulation of UII post-challenge (all P < 0.05). CONCLUSION:UII plays a role in the pathogenesis and priming of ALF by triggering an inflammatory cascade and driving the early release of cytokines in mice.
Authors: M Nowak; G C Gaines; J Rosenberg; R Minter; F R Bahjat; J Rectenwald; S L MacKay; C K Edwards; L L Moldawer Journal: Am J Physiol Regul Integr Comp Physiol Date: 2000-05 Impact factor: 3.619
Authors: Douglas G Johns; Zhaohui Ao; Diane Naselsky; Christopher L Herold; Kristeen Maniscalco; Lea Sarov-Blat; Klaudia Steplewski; Nambi Aiyar; Stephen A Douglas Journal: Naunyn Schmiedebergs Arch Pharmacol Date: 2004-09-30 Impact factor: 3.000