Catalpol Ameliorates Sodium Taurocholate-Induced Acute Pancreatitis in Rats via Inhibiting Activation of Nuclear Factor Kappa B

International Journal of Molecular Sciences

Wen Qin Xiao²  Guo Jian Yin²  Yu Ting Fan²  Lei Qiu²  Xiao Feng Cang²  Ge Yu¹  Yan Ling Hu²  Miao Xing²  De Qing Wu²  Xing Peng Wang¹  Guo Yong Hu² 

[1] Department of Gastroenterology, Shanghai First People’s Hospital, Shanghai Jiaotong University School of Medicine, 100 Haining Road, Hongkou District, Shanghai 200080, China; E-Mails:;Department of Gastroenterology, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, 301 Yanchang Road, Zhabei District, Shanghai 200072, China; E-Mails:

关键词: acute pancreatitis;    catalpol;    inflammatory cytokines;    NF-κB;   

DOI  :  10.3390/ijms150711957

来源: mdpi

【 摘 要 】

Catalpol, an iridoid glucoside extracted from the traditional Chinese herbal medicine, Rehmannia glutinosa, is reported to exert neuroprotective, anti-inflammatory, anti-tumor and anti-apoptotic effects. The main aim of the present study was to investigate whether catalpol ameliorates experimental acute pancreatitis (AP) induced by sodium taurocholate (STC). AP was induced in rats via retrograde injection of 4% STC (0.1 mL/100 g) into the biliopancreatic duct. Rats were pre-treated with saline or catalpol (50 mg/kg) 2 h before STC injection. At 12, 24 and 48 h after injection, the severity of AP was evaluated using biochemical and morphological analyses. Pretreatment with catalpol led to a significant reduction in serum amylase and lipase activities, pancreatic histological damage, myeloperoxidase (MPO) activity, interleukin (IL)-1β, IL-6 and TNF-α levels, and activation of nuclear factor kappa B (NF-κB). Moreover, administration of catalpol increased the viability of pancreatic acinar cells and inhibited NF-κB expression in vitro. Our results collectively support the potential of catalpol as a highly effective therapeutic agent for treatment of AP.

【 授权许可】

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© 2014 by the authors; licensee MDPI, Basel, Switzerland.