Effect of peroxisome proliferator-activated receptor-gamma ligand on inflammation of human gallbladder epithelial cells.

AIM: To investigate the effect of peroxisome proliferator-activated receptor gamma (PPAR-gamma) 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 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 microg/L of human interleukin-1beta (hIL-1beta) to make inflammatory model of HGBECs. The ciglitazone group was treated with various concentrations of ciglitazone, a potent ligand of PPAR-gamma. Subsequently, interleukin-8 (IL-8), IL-6, and tumor necrosis factor-alpha (TNF-alpha) 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-1beta. 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 (350.31+/-37.05 microg/L) than that in normal control group (50.0+/-0.00 microg/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.