Original Article
Copyright ©2011 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Apr 14, 2011; 17(14): 1825-1830
Published online Apr 14, 2011. doi: 10.3748/wjg.v17.i14.1825
Breviscapine attenuates acute pancreatitis by inhibiting expression of PKCα and NF-κB in pancreas
Hong Zhang, Cui-Zhu Cai, Xiao-Qin Zhang, Tao Li, Xiao-Yun Jia, Bao-Lan Li, Liang Song, Xiao-Jun Ma
Hong Zhang, Cui-Zhu Cai, Xiao-Qin Zhang, Tao Li, Xiao-Yun Jia, Bao-Lan Li, Liang Song, Xiao-Jun Ma, Department of Pathophysiology, Shaanxi University of Traditional Chinese Medicine, Xianyang 712046, Shaanxi Province, China
Cui-Zhu Cai, Department of Internal Medicine, Sanya Hospital of Traditional Chinese Medicine, Sanya 572000, Hainan Province, China
Author contributions: Zhang H and Cai CZ contributed equally to this work; Zhang H designed the research and wrote the paper; Cai CZ, Zhang XQ, Li T and Jia XY performed the research; Li BL, Song L and Ma XJ analyzed the data.
Supported by Funds of Natural Science of Shaanxi Education, No.05JK176; Natural Science of Shaanxi Province, No.2010JM4023 and Natural Science of Xianyang City, No. 2010K14-02(6)
Correspondence to: Hong Zhang, Professor, Department of Pathophysiology, Shaanxi University of Traditional Chinese Medicine, Xianyang 712046, Shaanxi Province, China. zhangh1227@sohu.com
Telephone: +86-29-38185120 Fax: +86-29-38185119
Received: November 10, 2010
Revised: January 11, 2011
Accepted: January 18, 2011
Published online: April 14, 2011
Abstract

AIM: To study the effect of breviscapine (Bre) on activity of protein kinase Cα (PKCα) and nuclear factor (NF)-κB in pancreas, and the mechanism of Bre attenuating acute pancreatitis (AP).

METHODS: One hundred and eight rats were randomly divided into acute necrotizing pancreatitis (ANP) group, Bre group (ANP + Bre group) and sham operation (SO) group, 36 rats in each group. ANP model was induced by a retrograde injection of 4% sodium deoxycholate into the bilio-pancreatic duct. Fifteen minutes after the ANP model was induced, the rats in Bre group were intraperitoneally injected with Bre (0.4 mg/100 g body weight or 0.1 mL/100 g body weight). Survival time and mortality of rats were calculated. Serum amylase and malondialdehyde levels were measured, volume of ascites was recorded and morphology of pancreas and lung was evaluated at 1, 5 and 10 h, after the ANP model was induced, respectively. Expressions of PKCα and subunit p65 of NF-κB in pancreas were detected by immunohistochemistry and Western blotting.

RESULTS: The life span of rats was longer and the mortality was lower in Bre group than in ANP group 13.51 ±5.46 vs 25.36 ± 8.11 (P < 0.05). The amylase and MDA levels as well as the volume of ascites were lower and the pathological changes in pancreas and lung were less in Bre group than ANP group (P < 0.05), indicating that the pancreatitis is less severe in Bre group than ANP group. The activation of PKCα and NF-κB p65 in pancreas was induced rapidly and reached their peak at 1 h or 5 h after ANP, but their activity in Bre group was significantly inhibited.

CONCLUSION: Bre exerts its therapeutic effect on AP by inhibiting the activation of PKCα and NF-κB p65 in pancreas.

Keywords: Breviscapine, Acute pancreatitis, Protein kinase Cα, Nuclear factor-κB, Rat