Brief Reports
Copyright ©The Author(s) 2005. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Oct 14, 2005; 11(38): 6061-6065
Published online Oct 14, 2005. doi: 10.3748/wjg.v11.i38.6061
Effect of peroxisome proliferator-activated receptor-gamma ligand on inflammation of human gallbladder epithelial cells
Guang-Dong Pan, Hong Wu, Jiang-Wen Liu, Nan-Sheng Cheng, Xian-Ze Xiong, Sheng-Fu Li, Guo-Fu Zhang, Lu-Nan Yan
Guang-Dong Pan, Hong Wu, Jiang-Wen Liu, Nan-Sheng Cheng, Xian-Ze Xiong, Lu-Nan Yan, Department of General Surgery, West China Hospital, Sichuan University, Chengdu 610041, Sichuan Province, China
Sheng-Fu Li, Laboratory of Transplant and Immunology, West China Hospital, Sichuan University, Chengdu 610041, Sichuan Province, China
Guo-Fu Zhang, Laboratory of Isotope, West China Hospital, Sichuan University, Chengdu 610041, Sichuan Province, China
Author contributions: All authors contributed equally to the work.
Supported by the Grants From the Scientific Research Foundation for Returned Overseas Chinese Scholars, Education Ministry of China, No. 2001-345
Correspondence to: Dr. Guang-Dong Pan, PO Box 119, West China Medical University, Chengdu 610041, Sichuan Province, China. pgdhx@126.com
Telephone: +86-28-88054973
Received: August 30, 2004
Revised: January 10, 2005
Accepted: January 14, 2005
Published online: October 14, 2005
Abstract

AIM: To investigate the effect of peroxisome proliferator-activated receptor gamma (PPAR-γ) and its ligand, ciglitazone, on inflammatory regulation of human gallbladder epithelial cells (HGBECs) and to assess the effect of human epithelial growth factor (hEGF) on growth of HGBECs.

METHODS: HGBECs were cultured in media containing hEGF or in hEGF-free media. HGBECs were divided into normal control group, inflammatory control group and ciglitazone group (test group). Inflammatory control group and ciglitazone group were treated with 5 mg/L of human interleukin-1β (hIL-1β) to make inflammatory model of HGBECs. The ciglitazone group was treated with various concentrations of ciglitazone, a potent ligand of PPAR-γ. Subsequently, interleukin-8 (IL-8), IL-6, and tumor necrosis factor-a (TNF-α) concentrations in all groups were measured. The data were analyzed statistically.

RESULTS: HGBECs were cultured in medium successfully. The longevity of HGBECs in groups containing hEGF was longer than that in hEGF-free groups. So was the number of HGBECs. The longest survival time of HGBEC was 25 d. The inflammatory model of HGBECs was obtained by treating with hIL-1β. The concentrations of IL-6 and IL-8 in ciglitazone group were lower than those in inflammatory control group (P<0.05). The secretion of IL-6 in inflammatory control group was higher (350.3137.05 mg/L) than that in normal control group (50.00.00 mg/L, P<0.001). Compared to normal control group, IL-8 concentration in inflammatory control was higher (P<0.05).

CONCLUSION: hEGF improves the growth of HGBECs in vitro. Ciglitazone inhibits the inflammation of HGBECs in vitro and has potential therapeutic effect on cholecystitis in vivo.

Keywords: PPAR-γ; Human gallbladder epithelial cells; Inflammation; Effect