Berberine inhibits inflammatory mediators and attenuates acute pancreatitis through deactivation of JNK signaling pathways. (June 2016)

• Record Type: Journal Article
• Authors: Choi, Sun-Bok; Bae, Gi-Sang; Jo, Il-Joo; Wang, Shaofan; Song, Ho-Joon; Park, Sung-Joo
• Is Part Of: Molecular immunology. Volume 74(2016:Jun.)
• Page Start: 27
• Page End: 38
• Publication Date: 2016-06
• Subjects: AP acute pancreatitis -- BBR Berberine -- CCK cholecystokinin -- HPRT hypoxanthine guanine phosphoribosyltransferase -- H&E hematoxylin and eosin -- IHC immunohistochemical -- Iκ-Bα inhibitory kappa B alpha -- IL interleukin -- iNOS inducible nitric oxide synthesis -- JNK c-Jun N-terminal kinases -- MAPK mitogen activated protein kinase -- mRNA Messenger RNA -- NF-κB nuclear factor kappa B -- PBS phosphate buffered saline -- SAP severe acute pancreatitis -- TNF tumor necrosis factor; Acute pancreatitis -- Berberine -- Cytokine -- iNOS -- JNK; Immunochemistry -- Periodicals; Molecular biology -- Periodicals; Immunochemistry -- Periodicals; Allergy and Immunology -- Periodicals; Molecular Biology -- Periodicals; Immunochimie -- Périodiques; Biologie moléculaire -- Périodiques; Immunochemistry; Molecular biology; Periodicals; Electronic journals; 571.96
• DOI: 10.1016/j.molimm.2016.04.011
• Languages: English
• ISSNs: 0161-5890

Abstract

Graphical abstract: Highlights: Berberine inhibited cerulein-induced acute pancreatitis. Berberine inhibited activation of the JNK signaling pathways in acute pancreatitis. Berberine inhibited inflammatory mediators production in acute pancreatitis. Berberine exerts anti-inflammatory effects on acute pancreatitis. Abstract: Acute pancreatitis (AP) is a life-threatening disease. Berberine (BBR), a well-known plant alkaloid, is reported to have anti-inflammatory activity in many diseases. However, the effects of BBR on AP have not been clearly elucidated. Therefore, the present study aimed to investigate the effects of BBR on cerulein-induced AP in mice. AP was induced by either cerulein orl -arginine. In the BBR treated group, BBR was administered intraperitoneally 1 h before the first cerulein orl -arginine injection. Blood samples were obtained to determine serum amylase and lipase activities and nitric oxide production. The pancreas and lung were rapidly removed for examination of histologic changes, myeloperoxidase (MPO) activity, and real-time reverse transcription-polymerase chain reaction. Furthermore, the regulating mechanisms of BBR were evaluated. Treatment of mice with BBR reduced pancreatic injury and activities of amylase, lipase, and pancreatitis-associated lung injury, as well as inhibited several inflammatory parameters such as the expression of pro-inflammatory cytokines and inducible nitric oxide synthesis (iNOS). Furthermore, BBR administration significantly inhibited c-Jun N-terminal kinase (JNK) activation in the cerulein-induced AP. Deactivation of JNK resulted in amelioration of pancreatitis and the inhibition of inflammatory mediators. These results suggest that BBR exerts anti-inflammatory effects on AP via JNK deactivation on mild and severe acute pancreatitis model, and could be a beneficial target in the management of AP.