• Pancreas · Jan 2014

    Opuntia humifusa ameliorated cerulein-induced acute pancreatitis.

    • Sun Bok Choi, Gi-Sang Bae, Kyoung-Chel Park, Il-Joo Jo, Seung-Hee Seo, Kyung Song, Dong-Sung Lee, Hyuncheol Oh, Youn-Chul Kim, Jong-Jin Kim, Yong Kook Shin, Jin-Han Park, Min-Jun Seo, Ho-Joon Song, and Sung-Joo Park.
    • From the *Department of Herbology, School of Oriental Medicine, †BK21 plus team, Professional graduate school of Oriental medicine, ‡Hanbang Body-fluid Research Center, §College of Pharmacy, and Institute of Pharmaceutical Research and Development, and ∥College of Pharmacy, Wonkwang University, Iksan, Jeonbuk; ¶ChungBuk Technopark Bio Center, Jecheon, #Foundation of industry-academy cooperation, Semyung University, ChungBuk; and **Department of Medicinal Herb, Gyeongju University, Gyeongbuk, South Korea.
    • Pancreas. 2014 Jan 1;43(1):118-27.

    ObjectiveThe aim of this study was to evaluate the effects of Opuntia humifusa (OH) on cerulein-induced acute pancreatitis (AP).MethodsAcute pancreatitis was induced via intraperitoneal injection of cholecystokinin analog cerulein (50 μg/kg). In the OH pretreatment group, OH was administered intraperitoneally (100, 250, or 500 mg/kg) 1 hour before first cerulein injection. In the posttreatment group, OH was administered intraperitoneally (500 mg/kg) 1 hour after the first cerulein injection. Furthermore, we isolated the pancreatic acinar cells using collagenase method, then investigated the acinar cell viability, cytokine productions, and the regulating mechanisms.ResultsThe both pretreatment and posttreatment of OH treatment attenuated the severity of AP, as shown by the histology of the pancreas and lung, and inhibited neutrophil infiltration; serum amylase and lipase activities; proinflammatory cytokine expression such as interleukin 1, interleukin 6, and tumor necrosis factor α; and cell death including apoptosis and necrosis. Furthermore, OH inhibited the activation of c-Jun N-terminal kinases.ConclusionsThese results suggest that OH reduces the severity of AP by inhibiting acinar cell death through c-Jun N-terminal kinases.

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