caa a22 4500 445887923 CHVBK 20180317145605.0 cr unu---uuuuu 170323e20110601xx s 000 0 eng 10.1007/s00535-011-0394-x doi (NATIONALLICENCE)springer-10.1007/s00535-011-0394-x Pomalidomide suppresses cerulein-induced acute pancreatitis in mice [Elektronische Daten] [Ming Tsai, Chinpiao Chen, Sung-Ho Chen, Yen Huang, Ted Chiu] Background: An overproduction of proinflammatory mediators in severe acute pancreatitis contributes to the systemic inflammatory response, which may lead to multiorgan damage and even death. Thus, inflammatory cytokines, e.g., tumor necrosis factor (TNF)-α and interleukin (IL)-1β, may be novel targets for the treatment of acute pancreatitis. The aim of this study was to investigate the therapeutic effects of pomalidomide (or CC-4047), a thalidomide analog and immunomodulatory agent, in acute pancreatitis. Methods: Acute pancreatitis was induced in C57BL/6 mice by intraperitoneal administration of cerulein (100μg/kg/h×8). Pomalidomide was administered (0.5mg/kg orally) 1h before the first or 1h after the last cerulein administration. The severity of the acute pancreatitis was evaluated biochemically and morphologically. Results: Pretreatment with pomalidomide significantly reduced the plasma levels of amylase and lipase; the histological injury; and the expression of TNF-α, IL-1β, monocyte chemotactic protein-1 (MCP-1), and inducible nitric oxide synthase (iNOS) in cerulein-induced acute pancreatitis. Post-treatment with pomalidomide also decreased the cerulein-induced elevation of plasma amylase and lipase and decreased the pancreatic damage. Conclusions: Treatment with pomalidomide ameliorated the severity of cerulein-induced acute pancreatitis in mice. Our data suggest that pomalidomide may become a new therapeutic agent in future clinical trials for the treatment of acute pancreatitis. Springer, 2011 Cerulein nationallicence Pancreatitis nationallicence Pomalidomide nationallicence CC-4047 nationallicence Cytokines nationallicence Tsai Ming Institute of Pharmacology and Toxicology, Tzu Chi University, 970, Hualien, Taiwan aut Chen Chinpiao Department of Chemistry, National Dong Hwa University, 974, Hualien, Taiwan aut Chen Sung-Ho Institute of Pharmacology and Toxicology, Tzu Chi University, 970, Hualien, Taiwan aut Huang Yen Institute of Pharmacology and Toxicology, Tzu Chi University, 970, Hualien, Taiwan aut Chiu Ted Institute of Pharmacology and Toxicology, Tzu Chi University, 970, Hualien, Taiwan aut Journal of Gastroenterology Springer Japan 46/6(2011-06-01), 822-833 0944-1174 46:6<822 2011 46 535 https://doi.org/10.1007/s00535-011-0394-x text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00535-011-0394-x text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Tsai Ming Institute of Pharmacology and Toxicology, Tzu Chi University, 970, Hualien, Taiwan aut NATIONALLICENCE 700 1- Chen Chinpiao Department of Chemistry, National Dong Hwa University, 974, Hualien, Taiwan aut NATIONALLICENCE 700 1- Chen Sung-Ho Institute of Pharmacology and Toxicology, Tzu Chi University, 970, Hualien, Taiwan aut NATIONALLICENCE 700 1- Huang Yen Institute of Pharmacology and Toxicology, Tzu Chi University, 970, Hualien, Taiwan aut NATIONALLICENCE 700 1- Chiu Ted Institute of Pharmacology and Toxicology, Tzu Chi University, 970, Hualien, Taiwan aut NATIONALLICENCE 773 0- Journal of Gastroenterology Springer Japan 46/6(2011-06-01), 822-833 0944-1174 46:6<822 2011 46 535 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer