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...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.展开更多
目的探讨苯扎贝特对THP1巨噬细胞PPARγ及ABCA1表达的影响。方法 THP1细胞经PMA诱导24h后,添加不同浓度苯扎贝特(0、1、10、50μmol/L)继续作用24h,RT-PCR法测定PPARγ、ABCA1 m RNA表达。结果 PMA刺激THP1细胞表达PPARγ及ABCA1;苯扎...目的探讨苯扎贝特对THP1巨噬细胞PPARγ及ABCA1表达的影响。方法 THP1细胞经PMA诱导24h后,添加不同浓度苯扎贝特(0、1、10、50μmol/L)继续作用24h,RT-PCR法测定PPARγ、ABCA1 m RNA表达。结果 PMA刺激THP1细胞表达PPARγ及ABCA1;苯扎贝特剂量依赖性上调THP-1巨噬细胞PPARγ及ABCA1的表达(P<0.05),50μmol/L浓度时二者表达最高,且PPARγ与ABCA1的m RNA表达呈正相关(r=0.628,P=0.002)。结论苯扎贝特上调THP1细胞中PPARγ和ABCA1的表达。展开更多
目的观察益气固表丸灌胃对慢性阻塞性肺疾病(COPD)小鼠内脏脂肪堆积、白色脂肪棕色化及代谢性炎症反应的影响,并探讨其可能的机制。方法将30只C57BL/6雄性小鼠随机分为空白对照组、COPD组、益气固表丸组,每组10只。COPD组、益气固表丸...目的观察益气固表丸灌胃对慢性阻塞性肺疾病(COPD)小鼠内脏脂肪堆积、白色脂肪棕色化及代谢性炎症反应的影响,并探讨其可能的机制。方法将30只C57BL/6雄性小鼠随机分为空白对照组、COPD组、益气固表丸组,每组10只。COPD组、益气固表丸组采用吸入香烟烟雾暴露联合香烟烟雾提取物腹腔注射的方法建立COPD模型;益气固表丸组于建模后灌胃给予益气固表丸溶解液200μL,1次/天,连续2周;空白对照组及COPD组给予等体积生理盐水灌胃。测算各组小鼠的Lee's指数及脂体比,处死后取肺组织和白色、棕色脂肪组织进行病理观察;采用Western blotting法检测白色脂肪组织棕色化相关指标[沉默信息调节因子1(SIRT1)、过氧化物酶体增殖物激活受体γ(PPARγ)、酶偶联蛋白1(UCP1)、过氧化物酶体增殖物活化受体γ共激活因子1α(PGC-1α)、PR结构域蛋白16(PRDM16)]及炎症反应相关指标[肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)、白细胞介素8(IL-8)]蛋白表达,免疫荧光法检测白色和棕色脂肪组织UCP1相对荧光强度,实时荧光定量PCR法检测白色脂肪组织TNF-α、IL-6、IL-8 m RNA表达,ELISA法检测血清IL-6、IL-8、TNF-α水平。结果COPD组小鼠肺组织可见较大面积肺泡壁轻度增厚,肺泡间隔增宽,炎症细胞浸润;益气固表丸组小鼠肺脏组织上述表现较COPD组减轻。与空白对照组比较,COPD组白色、棕色脂肪组织内的脂肪细胞体积均增大,细胞内空泡均增多;与COPD组比较,益气固表丸组白色、棕色脂肪组织内的脂滴减小,呈现出棕色化表现。与空白对照组比较,COPD组小鼠Lee's指数、脂体比及血清IL-6、IL-8、TNF-α水平均升高,白色脂肪组织TNF-α、IL-6、IL-8蛋白及m RNA相对表达量均升高,白色脂肪组织SIRT1、PPARγ、UCP1、PGC-1α、PRDM16蛋白相对表达量及白色、棕色脂肪组织UCP1相对荧光强度均降低(P均<0.05);与COPD组比较,益气固表丸组展开更多
基金Supported by the Grants From the Scientific Research Foundation for Returned Overseas Chinese Scholars, Education Ministry of China, No. 2001-345
文摘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.
文摘目的观察益气固表丸灌胃对慢性阻塞性肺疾病(COPD)小鼠内脏脂肪堆积、白色脂肪棕色化及代谢性炎症反应的影响,并探讨其可能的机制。方法将30只C57BL/6雄性小鼠随机分为空白对照组、COPD组、益气固表丸组,每组10只。COPD组、益气固表丸组采用吸入香烟烟雾暴露联合香烟烟雾提取物腹腔注射的方法建立COPD模型;益气固表丸组于建模后灌胃给予益气固表丸溶解液200μL,1次/天,连续2周;空白对照组及COPD组给予等体积生理盐水灌胃。测算各组小鼠的Lee's指数及脂体比,处死后取肺组织和白色、棕色脂肪组织进行病理观察;采用Western blotting法检测白色脂肪组织棕色化相关指标[沉默信息调节因子1(SIRT1)、过氧化物酶体增殖物激活受体γ(PPARγ)、酶偶联蛋白1(UCP1)、过氧化物酶体增殖物活化受体γ共激活因子1α(PGC-1α)、PR结构域蛋白16(PRDM16)]及炎症反应相关指标[肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)、白细胞介素8(IL-8)]蛋白表达,免疫荧光法检测白色和棕色脂肪组织UCP1相对荧光强度,实时荧光定量PCR法检测白色脂肪组织TNF-α、IL-6、IL-8 m RNA表达,ELISA法检测血清IL-6、IL-8、TNF-α水平。结果COPD组小鼠肺组织可见较大面积肺泡壁轻度增厚,肺泡间隔增宽,炎症细胞浸润;益气固表丸组小鼠肺脏组织上述表现较COPD组减轻。与空白对照组比较,COPD组白色、棕色脂肪组织内的脂肪细胞体积均增大,细胞内空泡均增多;与COPD组比较,益气固表丸组白色、棕色脂肪组织内的脂滴减小,呈现出棕色化表现。与空白对照组比较,COPD组小鼠Lee's指数、脂体比及血清IL-6、IL-8、TNF-α水平均升高,白色脂肪组织TNF-α、IL-6、IL-8蛋白及m RNA相对表达量均升高,白色脂肪组织SIRT1、PPARγ、UCP1、PGC-1α、PRDM16蛋白相对表达量及白色、棕色脂肪组织UCP1相对荧光强度均降低(P均<0.05);与COPD组比较,益气固表丸组
