摘要
AIM： To investigate the effect of peroxisome proliferatoractivated 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 μg/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-y. Subsequently, interleukin-8 （IL-8）, IL-6, and tumor necrosis factor-α （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 conlyol group （P〈0.05）. The secretion of IL-6 in inflammatory control group was higher （350.31±37.05 μg/L） than that in normal control group （50.0±0.00 μg/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.
AIM: To investigate the effect of peroxisome proliferatoractivated 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 μg/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-α (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 (350.31±37.05 μg/L) than that in normal control group (50.0±0.00 μg/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 HGBECsin vitro. Ciglitazone inhibits the inflammation of HGBECs in vitroand has potential therapeutic effect on cholecystitis in vivo.
基金
Supported by the Grants From the Scientific Research Foundation for Returned Overseas Chinese Scholars, Education Ministry of China, No. 2001-345
