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Effects of ciglitazone and troglitazone on the proliferation of human stomach cancer cells

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World Journal of Gastroenterology 2009年第3期15卷 310-320页

作者： Chan Woo Cheon Dae Hwan Kim Dong Heon Kim Yong Hoon Cho Jae Hun Kim Department of Surgery School of MedicineMedical Research InstitutePusan National UniversityBusan 602-739South Korea

AIM:To determine the cytological and molecular effects of peroxisome proliferation-activated receptor(PPAR)-γ and PPAR-γ agonists on stomach cancer ***:To determine the proliferation-suppressive effects of troglitazone and ciglitazone,SNU-216 and SNU-668 stomach cancer cells were plated in media containing 40 μmol/L troglitazone and ciglitazone at a density of 1 × 104 cells/*** 3,5 and 7 d,the cells were counted with a *** assess the appearance of PPAR-γ,a reverse-transcription polymerase chain reaction analysis was *** day 7,Western blotting was used to determine the effects of troglitazone and ciglitazone on the expression of p21 and phosphorylated-ERK(pERK) *** cytometry analysis was used to determine which portion of the cell cycle was delayed when troglitazone was used to suppress cell *** order to clarify the mechanism underlying the activity of troglitazone,microarray analysis was ***:PPAR-γ was manifested in both SNU-216 and SNU-668 *** and troglitazone suppressed cell growth,and troglitazone was a stronger suppressor of stomach cancer cells than ciglitazone,an inducer of cell cycle arrest in the G1 ***-668 cells were also determined to be more sensitive to ciglitazone and troglitazone than SNU-216 *** troglitazone and ciglitazone were administered to stomach cancer cells,levels of p21 expression were increased,but ERK phosphorylation levels were *** GW9662,an antagonist of PPAR-γ,was applied in conjunction with ciglitazone and troglitazone,the cell growth suppression effect was *** gene transcription program revealed a variety of alterations as the consequence of troglitazone treatment,and multiple troglitazone-associated pathways were *** genes whose expression was increased by troglitazone treatment were associated with cell development,differentiation,signal transmission between cells,and cell adhesion,and were also associated

关键词： Peroxisome proliferating-activated receptor-γ Ciglitazone troglitazone Stomach cancer cells

Reversal of P-glycoprotein-mediated Multidrug Resistance in SGC7901/VCR Cells by PPARγ Activation by troglitazone

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2010年第3期30卷 326-331页

作者：陈庆周洁蒋春舫陈娟 Department of Surgery Union HospitalTongji Medical CollegeHuazhong University of Science and Technology Department of Biochemistry and Molecular Biology School of Basic Medical SciencesTongji Medical CollegeHuazhong University of Science and Technology

Over-expression of P-glycoprotein(P-gp),an ATP-dependent drug efflux pump,represents one of the major mechanisms that contribute to multidrug resistance(MDR) in cancer *** study examined the effects of troglitazone,a ligand of peroxisome proliferator-activated receptor gamma(PPARγ),on P-gp-mediated MDR in SGC7901/VCR cells(a vincristine-resistant human gastric cancer cell line).The expression of P-gp was detected by RT-PCR and Western blotting,*** SGC7901/VCR cells were treated with 0.1 mg/L vincristine(VCR) alone or in combination with 1,5,10 μmol/L troglitazone for 24 ***γ was measured by electrophoretic mobility shift assay(EMSA).The intracellular concentration of Rhodamine123(Rh123,a fluorescent P-gp substrate) was assayed to evaluate the activity of *** cell cycle and apoptosis were measured by flow *** results showed that the P-gp was increasingly expressed in SGC7901,BGC823 and SGC7901/VCR cells in turn,suggesting that MDR in the SGC7901/VCR cells was mediated by the increased expression of *** the SGC7901/VCR cells,the expression level of total PPARγ was increased,however,the protein level and activity of PPARγ in the nuclei of cells decreased *** elevated the PPARγ activity in SGC7901/VCR cells in a dose-dependent *** decreased the P-gp expression and markedly enhanced the accumulation of Rh123 in SGC7901/VCR cells in a dose-dependent *** also found that troglitazone significantly increased the percentage of SGC7901/VCR cells in the G2/M phase and decreased the cell percentage in G1 and S phase in a dose-dependent *** significantly increased the apoptotic rate of SGC7901/VCR cells treated by VCR or ADR in a dose-dependent *** was concluded that P-gp-overexpressed SGC7901/VCR cells have minor endogenous PPARγ *** of the PPARγ activity by troglitazone can reverse P-gp-mediated MDR via down-regulating the expression and activity of P-gp i

关键词： multidrug resistance peroxisome proliferator-activated receptor gamma P-glycoprotein troglitazone SGC7901/VCR cells

Effect of troglitazone on Expression of Adhesion Molecules and eNOS in Human Saphenous Vein Gaft

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2007年第6期27卷 657-659页

作者：陈澍胡志伟张凯伦苏伟孙宗全 Department of Cardiovascular Surgery Union Hospital Tongji Medical College Huazhong University of Science and Technology

To investigate whether peroxisome proliferators-activated receptor-γ （PPARγ） ligand troglitazone can reduce endothelial injury and activation during storage of harvested saphenous vein grafts. Segments of human saphenous vein graft were collected from 9 patients undergoing coronary bypass surgery and then divided into two equal parts of control and test specimens, were stored in ei- ther heparinized blood （control group） or heparinized blood containing 20 μmol/L troglitazone （test group） for 1 h at room temperature. Tissue distribution and protein expression of VCAM-I, ICAM-I, and endothelial nitric oxide synthase （eNOS） were compared using immunohistochemistry and Western blot analysis. Myeloperoxidase （MPO） activity, a marker of neutrophil sequestration in human saphenous vein grafts, was also measured in each group. The expression of ICAM-1 （753±132 versus 7201±934; P〈0.01） , VCAM-1 （3731±294 versus 8292±793; P〈0.01）, and MPO activity （1.52±0.42 U/g, 5.04±1.26 U/g P〈0.01） were significantly lower in test group. In contract, eNOS expression （7983±834 versus 3989±1008; P〈0.01） was significantly higher in test group. PPARγ ligand troglitazone might reduce endothelial injury during the storage period of human saphenous vein grafts.

关键词： troglitazone adhesion molecule endothelial nitric oxide synthase saphenous vein graft

troglitazone, a peroxisome proliferator-activated receptor γ ligand, induces growth inhibition and apoptosis of HepG2 human liver cancer cells

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World Journal of Gastroenterology 2008年第14期14卷 2168-2173页

作者： Yan-Ming Zhou Yin-Hao Wen Xiao-Yan Kang Hai-Hua Qian Jia-Mei Yang Zheng-Feng Yin Department of Molecular Oncology Eastern Hepatobiliary Surgery Hospital Second Military Medical University Shanghai 200438 China

AIM: To examine the effect of troglitazone, a peroxisome proliferator-activated receptor γ (PPARγ) ligand, on the proliferation and apoptosis of human liver cancer cells. METHODS: Liver cancer cell line HepG2 was cultured and treated with troglitazone. Cell proliferation was detected by 3-(4-,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay; apoptosis was detected by flow cytometry and terminal deoxynucleotidyl transferase- mediated nick end labeling of DNA fragmentation sites (TUNEL) assay; and apoptosis-related protein was detected by immunocytochemistry and Western blotting. RESULTS: troglitazone inhibited growth and induced apoptosis of HepG2 cells in a dose-dependent manner, and induced activation of caspase-3 expression. troglitazone not only drove apoptosis-inhibiting factor survivin to translocate incompletely from the nucleus to the cytoplasm, but also inhibited expression of survivin, while it did not affect expression of apoptosis-promoting factor Bax. CONCLUSION: PPARγ ligands inhibit growth and induce apoptosis of liver cancer cells, and may have applications for the prevention and treatment of liver cancer.

关键词： Peroxisome proliferator-activated receptor γ troglitazone Liver neoplasms Apoptosis

troglitazone Induced Apoptosis via PPARγ Activated POX-induced ROS Formation in HT29 Cells

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Biomedical and Environmental Sciences 2011年第4期24卷 391-399页

作者： WANG Jing LV XiaoWen SHI JiePing HU XiaoSong DU YuGuo State Key Laboratory of Environmental Chemistry and Ecotoxicology Research Center for Eco-Environmental SciencesChinese Academy of SciencesBeijing 100085China Feed Research Institute Chinese Academy of Agricultural SciencesBeijing 100081China 3.College of Food Science and Nutritional EngineeringChina Agricultural UniversityBeijing 100083China College of Food Science and Nutritional Engineering China Agricultural University Beijing 100083 China

Objective In order to investigate the potential mechanisms in troglitazone-induced apoptosis in HT29 cells,the effects of PPARγ and POX-induced ROS were *** [3-（4,5）-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide （MTT） assay,Annexin V and PI staining using FACS,plasmid transfection,ROS formation detected by DCFH staining,RNA interference,RT-PCR RT-QPCR,and Western blotting analyses were employed to investigate the apoptotic effect of troglitazone and the potential role of PPARγ pathway and POX-induced ROS formation in HT29 *** troglitazone was found to inhibit the growth of HT29 cells by induction of *** this process,mitochondria related pathways including ROS formation,POX expression and cytochrome c release increased,which were inhibited by pretreatment with GW9662,a specific antagonist of PPARγ.These results illustrated that POX upregulation and ROS formation in apoptosis induced by troglitazone was modulated in PPARγ-dependent ***,the inhibition of ROS and apoptosis after POX siRNA used in troglitazone-treated HT29 cells indicated that POX be essential in the ROS formation and PPARγ-dependent apoptosis induced by *** The findings from this study showed that troglitazone-induced apoptosis was mediated by POX-induced ROS formation,at least partly,via PPARγ activation.

关键词： troglitazone Apoptosis HT29 POX ROS formation PPARγ Cytochrome c release

troglitazone对人腹膜间皮细胞TGF-β_1和纤维连接蛋白表达的影响

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中南大学学报（医学版） 2007年第3期32卷 473-479页

作者：刘虹彭佑铭刘伏友刘映红李玲艳李军陈星中南大学湘雅二医院肾内科中南大学肾病研究所长沙410011

目的:研究过氧化物增生体激活受体γ(PPAR-γ)激动剂troglitazone(曲格列酮,TGZ)对高浓度葡萄糖刺激下体外培养的人腹膜间皮细胞(HPMCs)中TGF-β1和细胞外基质纤维连接蛋白(Fn)表达的影响。方法:采用胰蛋白酶消化法从人大网膜组织中分... 详细信息

目的:研究过氧化物增生体激活受体γ(PPAR-γ)激动剂troglitazone(曲格列酮,TGZ)对高浓度葡萄糖刺激下体外培养的人腹膜间皮细胞(HPMCs)中TGF-β1和细胞外基质纤维连接蛋白(Fn)表达的影响。方法:采用胰蛋白酶消化法从人大网膜组织中分离间皮细胞,建立稳定的体外培养模型。根据细胞增殖与毒性实验选择troglitazone的最佳浓度15μmol/L,干预高浓度葡萄糖(30mmol/LD-葡萄糖)刺激下的人腹膜间皮细胞。采用逆转录多聚酶链式反应(RT-PCR)半定量检测HPMCs中PPAR-γ,TGF-β1以及Fn的 mRNA表达;采用双抗夹心法酶联免疫吸附实验检测HPMCs培养液中TGF-β1蛋白质水平;Western印迹检测Fn蛋白质水平。结果:高糖(30mmol/LD-葡萄糖)刺激可在 mRNA和蛋白质水平明显上调HPMCs表达TGF-β1和Fn(Ptroglitazone干预高糖孵育的HPMCs,可使TGF-β1和Fn mRNA和蛋白质的表达明显下调(Ptroglitazone能够明显抑制在高糖刺激下的HPMCsTGF-β1和Fn的表达,这可能为临床防治长期腹膜透析患者的腹膜纤维化提供一种较为有效的方法。

关键词： PPAR-γ troglitazone 人腹膜间皮细胞转化生长因子-β1 纤维连接蛋白

troglitazone对高糖和LPS诱导的人肾小球mPGEs蛋白表达的抑制作用

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中南大学学报（医学版） 2004年第3期29卷 297-300页

作者：凌光辉彭佑铭王海涛段绍斌刘映红刘伏友中南大学湘雅二医院肾内科长沙410011 广州军区总医院肾内科广州510000

目的 :研究PPAR γ激动剂troglitazone对LPS或高浓度葡萄糖作用的体外培养的人肾小球mPGEs蛋白表达水平的影响。方法 :用LPS或高浓度葡萄糖分别与不同浓度troglitazone作用体外培养的人肾小球 ,ELISA法检测上清液中mPGEs浓度。结果 :LPS... 详细信息

目的 :研究PPAR γ激动剂troglitazone对LPS或高浓度葡萄糖作用的体外培养的人肾小球mPGEs蛋白表达水平的影响。方法 :用LPS或高浓度葡萄糖分别与不同浓度troglitazone作用体外培养的人肾小球 ,ELISA法检测上清液中mPGEs浓度。结果 :LPS(10 μg/ml)或 5 %葡萄糖均可使体外培养的人肾小球mPGEs明显增高。 10～ 2 0nmol/L的troglitazone可明显抑制LPS(10 μg/ml)和 5 %葡萄糖诱导的大鼠系膜细胞mPGEs蛋白表达水平的增高 (P <0 .0 5 )。结论 :LPS和 5 %葡萄糖可诱导体外培养的人肾小球mPGEs蛋白表达水平明显增高 ,PPAR γ激动剂troglita zone可明显抑制两者所诱导的体外培养的人肾小球mPGEs蛋白表达水平的增高。

关键词： troglitazone 高糖 LPS诱导肾小球 mPGEs蛋白基因表达抑制作用受体基因

Effect of ligand troglitazone on peroxisome proliferator-activated receptor γ expression and cellular growth in human colon cancer cells

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World Journal of Gastroenterology 2006年第45期12卷 7263-7270页

作者： Mei Ming Jie-Ping Yu Xiang-Zhi Meng Yan-Hong Zhou Hong-Gang Yu He-Sheng kuo Department of Gastroenterology Renmin Hospital of Wuhan University Wuhan 430060 Hubei Province China Department of Pathophysiology and Pathology Medical College of Wuhan University Wuhan 430071 Hubei Province China

AIM： To investigate the effect of troglitazone on peroxisome proliferator-activated receptor γ （PPARγ） expression and cellular growth in human colon cancer HCT-116 and HCT-15 cells and to explore the related molecular mechanism.METHODS： Human colon cancer HCT-116 and HCT-15 cells cultured in vitro were treated with troglitazone. Reverse transcription-polymerase chain reaction （RT-PCR） and Western blot were employed to detect the effect of troglitazone on PPARy expression. The proliferative activity was determined by MTT assay, cell cycle and apoptosis were detected by flow cytometry. Apoptosisrelated genes, cell cycle regulatory genes and p53 were examined by RT-PCR and Western blot respectively. RESULTS： The expression of PPARy in colon cancer HCT-116 and HCT-15 cells was up-regulated by troglitazone. troglitazone inhibited proliferation, induced apoptosis and cell cycle G1 arrest in colon cancer cells. troglitazone induced p53 expression in HCT-116 cells, but not in HCT-15 cells. The down-regulation of survivin and bcl-2 was found in both cell lines and up-regulation of bax was found only in HCT-116 cells, being consistent with growth inhibition in HCT-116 cells but not in HCT-15 cells. troglitazone increased expression of p21^WAF1/CIP1 （p21）, p27^KIP1 （p27） and reduced cyclin D1 in HCT-116 cells while only a minor decrease of cyclin D1 was found in HCT-15 cells. CONCLUSION： troglitazone is an inductor of PPARγ in colon cancer cells and inhibits PPARγ-dependently proliferation, which may attribute to cell cycle G1 arrest and apoptosis in colon cancer cells. troglitazone may induce p53-independent apoptosis and p53- dependent expression of p21 and p27. Depending on cell background, different activation pathways may exist in colon cancer cells.

关键词： Peroxisome proliferator-activated receptor γ Colon cancer troglitazone Cellular growth Cell cycle Apoptosis

troglitazone对小鼠Ⅰ型葡萄糖载体表达的影响

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时珍国医国药 2005年第10期16卷 949-950页

作者：李天洙柳明洙延边大学医学院吉林延吉133000 延边大学医学院

目的:探讨troglitazone对小鼠I型葡萄糖载体(mGLUT1)表达的影响。方法:采用分子克隆技术,将过氧化物酶体增殖物受体γ(PPARγ)和维甲酸类受体X(RXRα)及mGLUT1 cDNA分别克隆到表达载体pCMX和pGL3b上。PPARγ与RXRα及mGLUT1克隆载体转染... 详细信息

目的:探讨troglitazone对小鼠I型葡萄糖载体(mGLUT1)表达的影响。方法:采用分子克隆技术,将过氧化物酶体增殖物受体γ(PPARγ)和维甲酸类受体X(RXRα)及mGLUT1 cDNA分别克隆到表达载体pCMX和pGL3b上。PPARγ与RXRα及mGLUT1克隆载体转染NIH 3T3细胞,处理或不处理troglitazone,应用荧光素酶活性测定法及RNA印迹等方法测定troglitazone对mGLUT1重组体荧光素酶活性调节及对mRNA表达的影响。结果:troglitazone可激活mGLUT1重组体荧光素酶的活性,并且可增加mGLUT1的mRNA表达水平。结论:troglitazone可增强mGLUT1的表达,可能参与PPARγ对mGLUT1的调节过程。

关键词： troglitazone 小鼠Ⅰ型葡萄糖载体 mRNA表达