Rapid Communication
Copyright ©2006 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Jul 14, 2006; 12(26): 4232-4236
Published online Jul 14, 2006. doi: 10.3748/wjg.v12.i26.4232
Effect of Tetrandrine on LPS-induced NF-κB activation in isolated pancreatic acinar cells of rat
Hong Zhang, Yong-Yu Li, Xian-Zhong Wu
Hong Zhang, Department of Pathophysiology, Shaanxi College of Chinese Traditional Medicine, Xianyang 712046, Shaanxi Province, China
Yong-Yu Li, Department of Pathophysiology, Medical College of Tongji University, Shanghai 200092, China
Xian-Zhong Wu, Tianjin Medical University, Tianjin 300070, China
Author contributions: All authors contributed equally to the work.
Supported by the National Natural Science Foundation of China, No. 30370643
Correspondence to: Professor Yong-Yu Li, Department of Pathophysiology, Medical College of Tongji University, Shanghai 200092, China. zhangh1227@sohu.com
Telephone: +86-21-65985447
Received: December 29, 2005
Revised: February 10, 2006
Accepted: February 18, 2006
Published online: July 14, 2006
Abstract

AIM: To investigate the effect of Tetrandrine (Tet) on LPS-induced NF-κB activation and cell injury in pancreatic acinar cells and to explore the mechanism of Tetrandrine preventing LPS-induced acinar cell injury.

METHODS: Male rat pancreatic acinar cells were isolated by collagenase digestion, then exposed to LPS (10 mg/L), Tet (50 μmol/L, 100 μmol/L) or normal media. At different time point (30 min, 1 h, 4 h, 10 h) after treatment with the agents, cell viability was determined by MTT, the product and nuclear translocation of subunit p65 of NF-κB was visualized by immunofluorescence staining and nuclear protein was extracted to perform EMSA which was used to assay the NF-κB binding activity.

RESULTS: LPS induced cell damage directly in a time dependent manner and Tet attenuated LPS-induced cell damage (50 μmol/L, P < 0.05; 100 μmol/L, P < 0.01). NF-κB p65 immunofluorescence staining in cytoplasm increased and began showing its nuclear translocation within 30 min and the peak was shown at 1 h of LPS 10 mg/L treatment. NF-κB DNA binding activity showed the same alteration pattern as p65 immunofluorescence staining. In Tet group, the immunofluorescence staining in cytoplasm and nuclear translocation of NF-κB were inhibited significantly.

CONCLUSION: NF-κB activation is an important early event that may contribute to inflammatory responses and cell injury in pancreatic acinar cells. Tet possesses the protective effect on LPS-induced acinar cell injury by inhibiting NF-κB activation.

Keywords: Tetrandrine; Lipopolysaccharide; Pancreas; Acinar cells; NF-κB