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褪黑激素对CHL细胞过氧化DNA断裂的防护作用
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作者 薛丽君 金中初 《卫生毒理学杂志》 CSCD 1998年第4期233-234,共2页
DNA氧化性损伤同衰老及许多年龄相关疾病(肿瘤,心血管疾病)关系密切[1]。据报道,褪黑激素(Melatonin,MT)参与哺乳类细胞许多重要的生理病理过程的调节,如矫正生物钟紊乱,增强免疫,抗氧化作用等[2]。DN... DNA氧化性损伤同衰老及许多年龄相关疾病(肿瘤,心血管疾病)关系密切[1]。据报道,褪黑激素(Melatonin,MT)参与哺乳类细胞许多重要的生理病理过程的调节,如矫正生物钟紊乱,增强免疫,抗氧化作用等[2]。DNA链断裂是常见的过氧化损伤类型,为... 展开更多
关键词 褪黑激素 CHL 细胞过氧 防护作用 DNA 断裂
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Influence of Ciglitazone on HepG2 Cells Growth in Vitro and in Vivo and Its Mechanisms
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作者 潘华锋 陈孝平 《The Chinese-German Journal of Clinical Oncology》 CAS 2006年第3期169-172,共4页
Objective: To study the effect of ciglitazone on hepatic cancer cells HepG2 growth in vitro and in vivo and its mechanisms. Methods: The in vitro cultured HepG2 lines were treated with various concentrations of cigl... Objective: To study the effect of ciglitazone on hepatic cancer cells HepG2 growth in vitro and in vivo and its mechanisms. Methods: The in vitro cultured HepG2 lines were treated with various concentrations of ciglitazone. The in vitro growth of HepG2 cells was examined by growth curve and the cell cycle was analyzed by flow cytometry. HepG2 cells (1×10^6 /mouse) were inoculated subcutaneously into 20 nude mice to establish the hepatocellular carcinoma model. The mice were randomly divided into two groups: the control group (group A, n=10) and the ciglitazone-treated group (group B, n=10). The mice in the group B were injected with 100μL (100μmol/L) of ciglitazone every other day for 15 times, while the mice in the group A with saline instead. One month later, the weights of the resected subcutaneous tumors and suppression rates were measured. The expression of cyclinD1 and P21 was detected by Western blot. Results: The proliferation of HepG2 was significantly inhibited by ciglitazone in a dose- and timedependant manner. There were more cells arrested in G1/G0 phase and the expression of PPARγ was markedly up-regulated in HepG2 cells treated with ciglitazone. After the treatment with ciglitazone, the average weights of the tumors in the group A and B were 3.73±0.22 g and 2.60±0.35 g, respectively, and the tumor suppression rate in the group B was 30%. The expression of cyclinD1 was increased significantly, while that of P21 was decreased significantly in group A as compared with that in group B. Conclusion: Ciglitazone could significantly inhibit HepG2 proliferation in a dose- and time-dependent manner, and induce differentiation of HepG2, the mechanism of which may be related to the PPARγ intervention to cell cycle control. 展开更多
关键词 peroxisome proliferator-activated receptor γ CIGLITAZONE CYCLIND1 P21
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Troglitazone, a peroxisome proliferator-activated receptor γ ligand, induces growth inhibition and apoptosis of HepG2 human liver cancer cells 被引量:10
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作者 Yan-Ming Zhou Yin-Hao Wen Xiao-Yan Kang Hai-Hua Qian Jia-Mei Yang Zheng-Feng Yin 《World Journal of Gastroenterology》 SCIE CAS CSCD 2008年第14期2168-2173,共6页
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 cu... 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. 展开更多
关键词 Peroxisome proliferator-activated receptor γ TROGLITAZONE Liver neoplasms APOPTOSIS
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Blockage of PPARδ increases the expression of inflammatory factors in 3T3-L1 cells stimulated with TNFα 被引量:2
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作者 张莉莉 祝之明 +1 位作者 曹廷兵 王利娟 《Journal of Medical Colleges of PLA(China)》 CAS 2006年第2期77-81,共5页
Objective: To investigate the role of peroxisome proliferator-activated receptors δ (PPARδ) in inflammatory reaction and its possible mechanism in adipocyte. Methods:Lentivirus-mediated RNA interference (RNAi)... Objective: To investigate the role of peroxisome proliferator-activated receptors δ (PPARδ) in inflammatory reaction and its possible mechanism in adipocyte. Methods:Lentivirus-mediated RNA interference (RNAi) was used to block the expression of PPARδ in 3T3-L1 cells. In order to induce inflammation in 3T3-L1, cells were stimulated with tumor necrosis factor-α(TNFα, 20 ng/ml) for 4 h. The expression of PPARδ, nuclear factor κB (NFκB) and C reactive protein (CRP) were determined by Western blot analysis. Results:The expression of PPARδ was reduced by 80% after RNAi. Blockage of PPARδ promoted the expression of CRP and NFκB in cells stimulated with TNFα but had no effect on normal cells. Conclusion: PPARδ is involved in inflammatory reaction in adipocyte. Blockage of PPARδ can promote the inflammation mediated by inflammatory factors and increase the expression of NFκB and CRP in 3T3-L1 cells stimulated with TNFα. 展开更多
关键词 RNA interference 3T3-L1 cells peroxisome proliferator-activated receptors 8 nuclear factor κB C reactive protein
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Induction of defence gene expression by oligogalacturonic acid requires in-creases in both cytosolic calcium and hydrogen peroxide in Arabidopsis thaliana 被引量:4
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作者 XiangYangHU StevenJNEILL +1 位作者 WeiMingCAI ZhangChengTANG 《Cell Research》 SCIE CAS CSCD 2004年第3期234-240,共7页
Responses to oligogalacturonic acid (OGA) were determined in transgenic Arabidopsis thaliana seedlings expressing the calcium reporter protein aequorin. OGA stimulated a rapid, substantial and transient increase in th... Responses to oligogalacturonic acid (OGA) were determined in transgenic Arabidopsis thaliana seedlings expressing the calcium reporter protein aequorin. OGA stimulated a rapid, substantial and transient increase in the concentration of cytosolic calcium ([Ca2+]cyt) that peaked after ca. 15 s. This increase was dose-dependent, saturating at ca. 50 μg Gal equiv/ml of OGA. OGA also stimulated a rapid generation of H2O2. A small, rapid increase in H2O2 content was followed by a much larger oxidative burst, with H2O2 content peaking after ca. 60 min and declining thereafter. Induction of the oxidative burst by OGA was also dose-dependent, with a maximum response again being achieved at ca. 50 μg Gal equiv/mL. Inhibitors of calcium fluxes inhibited both increases in [Ca2+]cyt and [H2O2], whereas inhibitors of NADPH oxidase blocked only the oxidative burst. OGA increased strongly the expression of the defence-related genes CHS,GST, PAL and PR-1. This induction was suppressed by inhibitors of calcium flux or NADPH oxidase, indicating that increases in both cytosolic calcium and H2O2 are required for OGA-induced gene expression. 展开更多
关键词 Arabidopsis thaliana cytosolic calcium defence gene expression hydrogen peroxide OGA.
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Polaprezinc protects human colon cells from oxidative injury induced by hydrogen peroxide:Relevant to cytoprotective heat shock proteins 被引量:3
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作者 Tatsuya Ohkawara Jun Nishihira +2 位作者 Rika Nagashima Hiroshi Takeda Masahiro Asaka 《World Journal of Gastroenterology》 SCIE CAS CSCD 2006年第38期6178-6181,共4页
AIM: To investigate the effect of polaprezinc on cellular damage induced by hydrogen peroxide (H202) in human colon CaCo2 cells. METHODS: CaCo2 cells were treated with polaprezinc (10-100 pmol/L) for 6 h. After ... AIM: To investigate the effect of polaprezinc on cellular damage induced by hydrogen peroxide (H202) in human colon CaCo2 cells. METHODS: CaCo2 cells were treated with polaprezinc (10-100 pmol/L) for 6 h. After polaprezinc treatment, the cells were incubated with H202 (20μmol/L) for 1 h. Cell viability was measured by MTT assay. Western blot analysis for heat shock protein (HSP) 27 and HSP72 in the cells was performed. Moreover, cells were pretreated with quercetin (200 μmol/L), an inhibitor of HSP synthesis, 2 h before polaprezinc treatment, and cell viability and the expression of HSP27 and 72 were assessed in these cells. RESULTS: Polaprezinc significantly protected CaCo2 cells from cell damage induced by H2O2, and up-regulated the expressions of HSP27 and HSP72 in the cells (10, 30 and 100 pmol/L of polaprezinc; 35.0% ± 7.7%, 58.3% ± 14.6% and 64.2% ± 8.2%, respectively. P 〈 0.01 versus polaprezinc-nontreated cells; 6.0% ± 4.4%). Quercetin inhibited the up-regulation of HSP27 and HSP72 by polaprezinc and diminished the protective effect of polaprezinc against H2O2-caused injury in the cells. CONCLUSION: Polaprezinc is a useful therapeutic agent for treatment of colitis and its effects depend on the function of cytoprotective HSP in colon. 展开更多
关键词 Heat shock protein Oxidative injury POLAPREZINC
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Protective effects of non-mitogenic human acidic fibroblast growth factor on hydrogen peroxide-induced damage to cardiomyocytes in vitro 被引量:6
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作者 Zhuo-Feng Lin Xiao-Kun Li +3 位作者 Yuan Lin Fan Wu Li-Min Liang Xiao-Bing Fu 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第35期5492-5497,共6页
AIM: To study the protective effect of non-mitogenic human acidic fibroblast growth factor (FGF) on cardiac oxidative injury in vivo. METHODS: Ventricular cardiomyocytes were isolated from 1- to 3-d-old neonatal S... AIM: To study the protective effect of non-mitogenic human acidic fibroblast growth factor (FGF) on cardiac oxidative injury in vivo. METHODS: Ventricular cardiomyocytes were isolated from 1- to 3-d-old neonatal SD mice and cultured in Dulbecco's minimum essential medium supplemented with 15% fetal bovine serum under an atmosphere of 50 mL/L CO2-95% air at 37℃, as well as assessed by immunooltochemical assay. We constructed the cardiomyoolte injury model by exposure to a certain concentration of H2O2. Cellular viability, superoxide dismutase (SOD) activity, leakage of maleic dialdehyde and anti-apoptosis effect were included to evaluate the cardiac protective effect of non-mitogenic human acidic FGF. RESULTS: Over 50% of the cardiomyocytes beat spontaneously on the 2nd d of culture and synchronously beat after being cultured for 3 d. Forty-eight hours after plating was completed, the purity of such cultures was 95% myocytes, assessed by an immunocytochemical assay. Cellular viability dramatically decreased with the increasing of the concentration of H2O2. Non-mitogenic human acidic FGF showed significant resistance to thetoxic effect of H2O2, significantly increased the cellular viability as well as the activity of SOD, and dramatically decreased the leakage of maleic dialdehyde as well as the cellular apoptosis rate. CONCLUSION: Hydrogen peroxide shows strong cytotoxicity to the cultured cardiac myocytes, and non-mitogenic human acidic FGF shows strong cardio-protective effect when exposed to a certain concentration of H2O2. 展开更多
关键词 Non-mitogenic human acidic fibroblast growthfactor CARDIOPROTECTION Cardiomyooltes H2O2
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Generation of Reactive Oxygen Species in Different Fractions of the Coelomocytes of Holothurian Eupentacta fraudatrix in Response to the Thermostable Toxin of Yersinia pseudotuberculosis in Vitro 被引量:3
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作者 Dolmatova L. S. +7 位作者 Eliseykina M. G. Timchenko N. F. Kovaleva A. L. Shitkova O. A 《Chinese Journal of Oceanology and Limnology》 SCIE CAS CSCD 2003年第4期293-304,共12页
Pure fraction (92%-95%) of phagocytes (FP) and a mixture of amoebocytes(62%) and morula cells (38 %) FPMC of the holothurian Eupentacta fraudatrix (Holothuroidea, Dendrochirota) were obtained by using ficoll verograph... Pure fraction (92%-95%) of phagocytes (FP) and a mixture of amoebocytes(62%) and morula cells (38 %) FPMC of the holothurian Eupentacta fraudatrix (Holothuroidea, Dendrochirota) were obtained by using ficoll verographine step gradient. Basal production of reactive oxygen species (ROS) in FP quantified by using reduction of nitroblue tetrazolium (NBT) was more than twice that in FPMC. Thermostable toxin of Yersinia pseudotuberculosis (TST) at different concentrations ( 0.2; 0.5; 2.5 μg/ml, but not 0.1 μg/ml) stimulated NBT reduction in FPMC after 24 h incubation. In FP, TST at concentrations of 0.1 and 0.2 μg/ml inhibited and at concentrations of 0.5 and 2.5 μg/ml stimulated NBT reduction after 24 h incubation. Maximal effect was observed in FP and FPMC at TST concentrations of 0.5 and 0.2 μg/ml, respectively. Addition of catalase (0.7 μg/ml) to the cells treated with TST (2.5 μg/ml) was followed by a decrease in NBT reduction compared to that under toxin treatment alone. TST stimulated superoxide dismutase activity in concentration dependent manner (maximum at 0.5 μg/ml concentration in FP) after 24 h treatment, and this stimulation was prevented by a commercial catalase. Plant lectin concanavalin A stimulated NBT reduction more than 5 fold in FPMC compared to the control. With addition of TST, lectin stimulated ROS to lesser extent than that with lectin alone. When catalase, TST, and lectin were added into the FPMC simultaneously, ROS increase was similar to that under lectin treatment alone. On the whole, data obtained indicated that ROS generation in holothurian coelomocytes especially occurs in both stimulated and not stimulated phagocytes, and that changes in ROS production by these cells may be one of the mechanisms of antibacterial protection of holothurians. 展开更多
关键词 bacterial toxin COELOMOCYTES HOLOTHURIAN reactive oxygen species superoxide dismutase
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DNA damage-induced cell death: lessons from the central nervous system 被引量:4
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作者 Helena Lobo Borges Rafael Linden Jean YJ Wang 《Cell Research》 SCIE CAS CSCD 2008年第1期17-26,共10页
DNA damage can, but does not always, induce cell death. While several pathways linking DNA damage signals to mitochondria-dependent and -independent death machineries have been elucidated, the connectivity of these pa... DNA damage can, but does not always, induce cell death. While several pathways linking DNA damage signals to mitochondria-dependent and -independent death machineries have been elucidated, the connectivity of these pathways is subject to regulation by multiple other factors that are not well understood. We have proposed two conceptual models to explain the delayed and variable cell death response to DNA damage: integrative surveillance versus autonomous pathways. In this review, we discuss how these two models may explain the in vivo regulation of cell death induced by ionizing radiation (IR) in the developing central nervous system, where the death response is regulated by radiation dose, cell cycle status and neuronal development. 展开更多
关键词 apoptosis ATM ionizing radiation neonatal retina NEUROBLASTS p53 phosphorylation
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Apoptosis of pancreatic cancer BXPC-3 cells induced by indole-3-acetic acid in combination with horseradish peroxidase 被引量:5
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作者 Chen Huang Li-Ying Liu +7 位作者 Tu-Sheng Song Lei Ni Ling Yang Xiao-Yan Hu Jing-Song Hu Li-Ping Song Yu Luo Lu-Sheng Si 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第29期4519-4523,共5页
AIM: To explore the mechanisms underlying the apoptosis of human pancreatic cancer BXPC-3 cells induced by indole-3-acetic acid (IAA) in combination with horseradish peroxidase (HRP). METHODS: BXPC-3 cells deriv... AIM: To explore the mechanisms underlying the apoptosis of human pancreatic cancer BXPC-3 cells induced by indole-3-acetic acid (IAA) in combination with horseradish peroxidase (HRP). METHODS: BXPC-3 cells derived from human pancreatic cancer were exposed to 40 or 80 μmol/L IAA and 1.2 μg/mL HRP at different times. Then, Mn- assay was used to detect the cell proliferation. Flow cytometry was performed to analyze cell cycle. Terminal deoxynucleotidyl transferasemediated dUTP nick end labeling assay was used to detect apoptosis. 2,7-Dichlorofluorescin diacetate uptake was measured by confocal microscopy to determine free radicals. Level of malondialdehyde (MDA) and activity of superoxide dismutase (SOD) were measured by biochemical methods. RESULTS: IAA/HRP initiated growth inhibition of BXPC-3 cells in a dose- and time-dependent manner. Flow cytometry revealed that the cells treated for 48 h were arrested at G1/G0. After exposure to 80 μmol/L IAA plus 1.2 μg/mL HRP for 72 h, the apoptosis rate increased to 72.5‰, which was nine times that of control. Content of MDA and activity of SOD increased respectively after treatment compared to control. Meanwhile, IAA/HRP stimulated the formation of free radicals. CONCLUSION: The combination of IAA and HRP can inhibit the growth of human pancreatic cancer BXPC-3 cells in vitro by inducing apoptosis. 展开更多
关键词 Indole-3-acetic acid Horseradish peroxidase BXPC-3 cells APOPTOSIS Free radical
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Role of MGST1 in reactive intermediate-induced injury 被引量:3
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作者 Courtney S Schaffert 《World Journal of Gastroenterology》 SCIE CAS CSCD 2011年第20期2552-2557,共6页
Microsomal glutathione transferase (MGST1, EC 2.5.1.18) is a membrane bound glutathione transferase extensively studied for its ability to detoxify reactive intermediates, including metabolic electrophile intermediate... Microsomal glutathione transferase (MGST1, EC 2.5.1.18) is a membrane bound glutathione transferase extensively studied for its ability to detoxify reactive intermediates, including metabolic electrophile intermediates and lipophilic hydroperoxides through its glutathione dependent transferase and peroxidase activities. It is expressed in high amounts in the liver, located both in the endoplasmic reticulum and the inner and outer mitochondrial membranes. This enzyme is activated by oxidative stress. Binding of GSH and modification of cysteine 49 (the oxidative stress sensor) has been shown to increase activation and induce conformational changes in the enzyme. These changes have either been shown to enhance the protective effect ascribed to this enzyme or have been shown to contribute to cell death through mitochondrial permeability transition pore formation. The purpose of this review is to elucidate how one enzyme found in two places in the cell subjected to the same conditions of oxidative stress could both help protect against and contribute to reactive oxygen species-induced liver injury. 展开更多
关键词 Microsomal glutathione transferase 1 Oxidative stress Mitochondrial permeability transition GLUTATHIONE Liver injury
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Protective Actions of Blumea Flavanones on Primary Cultured Hepatocytes and Liver Subcellular Organelle against Lipid Peroxidation
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作者 赵金华 许实波 +2 位作者 王正濂 林永成 陈荣礼 《Journal of Chinese Pharmaceutical Sciences》 CAS 1998年第3期40-44,共5页
To search for the protective actions of blumea flavanones (BFs) on hepatocytes and hepatic subcellular organelle against lipid peroxidation, monkey′s hepatocytes were isolated and cultured with or without blumea flav... To search for the protective actions of blumea flavanones (BFs) on hepatocytes and hepatic subcellular organelle against lipid peroxidation, monkey′s hepatocytes were isolated and cultured with or without blumea flavanones, then damaged by FeSO 4 cysteine or CCl 4. The lipid peroxidation (malondialdehyde production) and alteration in hepatocyte membrane (leakage of GPT) were estimated. Hepatic subcellular organelles were also isolated and incubated with or without blumea flavanones, then injured by FeSO 4 ascorbate. The generation of malondialdehyde(MDA) was measured. It was found that BFs 10 and 100 μmol·L 1 inhibited the MDA generation and GPT (glutamic pyruvic transaminase) leakage out of hepatocytes that were induced by CCl 4 or FeSO 4 cysteine. BFs could prevent lipid peroxidation initiated by FeSO 4 ascorbate in subcellular organelle suspension. Among BFs, BF 2 possessed the strongest activity. Conclusion: Blumea flavanones possess antioxidation activities that protect monkey′s hepatocytes and hepatic subcellular organelle against injuries induced by FeSO4 or CCl 4. 展开更多
关键词 Blumea flavanones Antioxidants Macaca mulatta HEPATOCYTE Subcellular organelle
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Curcumin suppresses PPARδ expression and related genes in HT-29 cells 被引量:2
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作者 Jin-Bo Wang Li-Li Qi +2 位作者 Shui-Di Zheng Heng-Zheng Wang Tian-Xing Wu 《World Journal of Gastroenterology》 SCIE CAS CSCD 2009年第11期1346-1352,共7页
AIM:To investigate the effects of curcumin on the expression of peroxisome proliferator-activated receptorδ(PPARδ)and related genes in HT-29 cells. METHODS:HT-29 cells were treated with curcumin (0-80μmol/L)for 24 ... AIM:To investigate the effects of curcumin on the expression of peroxisome proliferator-activated receptorδ(PPARδ)and related genes in HT-29 cells. METHODS:HT-29 cells were treated with curcumin (0-80μmol/L)for 24 h.The effects of curcumin on the morphology of HT-29 cells were studied by Hoechst 33342 staining.The activity of caspase-3 was determined using DEVD-p NA as substrate.The levels of peroxisome PPARδ,14-3-3εand vascular endothelial growth factor(VEGF)in HT-29 cells were determined by Western blotting analysis and their mRNA expression was determined by real-time quantitative RT-PCR. RESULTS:Treatment with 10-80μmol/L curcumin induced typical features of apoptosis and activated the caspase-3 in HT-29 cells.The expression of PPARδ, 14-3-3εand VEGF was reduced and the activity of β-catenin/Tcf-4 signaling was inhibited by curcumin treatment. CONCLUSION:Curcumin can induce apoptosis of HT-29 cells and down-regulate the expression of PPARδ,14-3-3εand VEGF in HT-29. 展开更多
关键词 CURCUMIN 14-3-3ε Peroxisome proliferator-activated receptorδ Vascular endothelial growth factor HT-29 cells
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Protective effects of Rheum tanguticum polysaccharide against hydrogen peroxide-induced intestinal epithelial cell injury 被引量:11
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作者 Lin-NaLiu Qi-BingMei LiLiu FengZhang Zhen-GuoLiu Zhi-PengWang Ru-TaoWang 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第10期1503-1507,共5页
AIM: To describe the effect of Rheum tanguticum polysaccharide (RTP) on hydrogen peroxide-induced human intestinal epithelial cell injury. METHODS: Hydrogen peroxide (100 μmol/L) was introduced to induce human intest... AIM: To describe the effect of Rheum tanguticum polysaccharide (RTP) on hydrogen peroxide-induced human intestinal epithelial cell injury. METHODS: Hydrogen peroxide (100 μmol/L) was introduced to induce human intestinal epithelial cell injury. Cells were pretreated with RTP (30,100,300 μg/mL) for 24 h before exposure to hydrogen peroxide. Cell viability was detected by MTT assay and morphological observation. Acridine orange staining and flow cytometry were performed to assess cell apoptosis. Lactate dehydrogenase (LDH) activity, production of malondialdehyde (MDA) and superoxide dismutase (SOD) activity were measured by spectrophotometry with corresponding assay kits. RESULTS: Following exposure to H2O2, a marked decrease in cell survival and SOD activity, increased production of MDA, LDH leakage and cell apoptosis were found. Pretreatment of the cells with RTP could significantly elevate cell survival, SOD activity and decrease the level of MDA, LDH activity and cell apoptosis. CONCLUSION: RTP may have cytoprotective and anti-oxidant effects against H2O2-induced intestinal epithelial cell injury by inhibiting cell apoptosis and necrosis. This might be one of the possible mechanisms of RTP for the treatment of ulcerative colitis in rats. 展开更多
关键词 Rheum tanguticum polysaccharide Intestinal epithelial cells APOPTOSIS NECROSIS CATALASE
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Inhibitory Effect of Isorhapontigenin on Copper-Mediated Peroxidation of Human Low-Density Lipoprotein in vitro
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作者 方亚南 林茂 刘耕陶 《Journal of Chinese Pharmaceutical Sciences》 CAS 2004年第1期63-67,共5页
Aim To study the effect of Isorhapontigenin (Iso) on copper-mediatedperoxidation of human low-density lipoprotein (LDL) and on the toxicity of oxidized LDL (ox-LDL) tomouse macrophages in vitro. Methods Human LDL from... Aim To study the effect of Isorhapontigenin (Iso) on copper-mediatedperoxidation of human low-density lipoprotein (LDL) and on the toxicity of oxidized LDL (ox-LDL) tomouse macrophages in vitro. Methods Human LDL from sera df normal lipidemic donors was separated bysequential ultracentrifugation. The separated human IDL 1 mg·mL^(-1) in phosphate buffer saline, pH7.4, was incubated with cupric sulfate (10 μmol·L^(-1) ) at 37℃ for 10 h in the presence orabsence of various concentrations of Iso. Malondialdehyde (MDA) formation, vitamin E consumption,electrophoretic mobility of LDL, mitochondria] membrane potential of mouse peritoneal macrophages,phagocytosis of neutral red, and release of nitric oxide (NO) from macrophages were determined byvarious methods. Results Iso 1 - 100 μmol·L^(-1) significantly inhibited the increase of MDAformation, vitamin E consumption and electrophoretic mobility of LDL induced by Cu^(2+) in aconcentration-dependent manner. The injury of the mitochondrial membrane potential of mouseperitoneal macrophages due to incubation with ox-LDL (0.1 mg·mL^(-1)) at 37℃ for 12 h was markedlyprotected by 10 μmol·L^(-1) Iso. After pretreat-ment of the macrophages with 10 μmol · L^(-1)of Iso and then exposure to ox-LDL for 4 h, the reduction of phagocytosis of neutral red and releaseof NO in response to lipopolysaccharide (IPS) stimulation were significantly prevented. ConclusionIso has protective action against Cu^(2+) - mediated LDL peroxidation and ox-LDL induced toxicity tomacrophages in vitro. 展开更多
关键词 ISORHAPONTIGENIN low-density lipoprotein oxidized low-density lipoprotein MACROPHAGES PHAGOCYTOSIS mitochondrial membrane potential
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Somatic embryogenesis and peroxidase activity of desiccation tol-erant mature somatic embryos of loblolly pine 被引量:3
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作者 唐巍 《Journal of Forestry Research》 SCIE CAS CSCD 2001年第3期147-152,209,共6页
White, translucent, glossy mucilaginous callus was initiated from the mature zygotic embryos explants on callus induction medium with 2,4-D, BA, and kinetin in the 3-9th week of culture. This type of callus induction ... White, translucent, glossy mucilaginous callus was initiated from the mature zygotic embryos explants on callus induction medium with 2,4-D, BA, and kinetin in the 3-9th week of culture. This type of callus induction occurred at a lower fre-quency with either a-naphthaleneacetic acid (NAA) or IBA (both 8 mg/L). White, translucent, glossy mucilaginous callus was embryogenic and mainly developed from the cotyledons of the mature zygotic embryo. Somatic embryos were formed on dif-ferentiation medium. Desiccation tolerance can be induced by culturing somatic embryos of loblolly pine (Pinus taeda L.) on medium supplemented with 50 mm abscisic acid (ABA) and/or 8.5% polyethylene glycol (PEG6000). Scanning electron micros-copy of desiccated somatic embryos showed that the size and external morphology of the desiccation tolerant somatic embryos recovered to the pre-desiccation state within 24-36 h, whereas the sensitive somatic embryos did not recover and remained shriveled, after the desiccated somatic embryos had been rehydrated. Peroxidase activity of desiccated somatic embryos in-creased sharply after 3 days of desiccation treatment, and desiccation tolerant somatic embryos had higher peroxidase activity compared to sensitive somatic embryos. Higher peroxidase activity of desiccation tolerant somatic embryos was possibly ad-vantage of catalyzing the reduction of H2O2 which was produced by drought stress, and protecting somatic embryos from oxida-tive damage. 展开更多
关键词 Pinus taeda L. Somatic embryogenesis Desiccation tolerance Peroxidase activity
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Protection of Salvianolic Acid B for Human Endothelial Cells Against Hydrogen Peroxide-Induced Oxidative Damage
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作者 张俊刚 赵广荣 +1 位作者 刘金玲 季祥武 《Transactions of Tianjin University》 EI CAS 2009年第6期434-439,共6页
Salvianolic acid B(Sal B) is an active component of traditional Chinese medicine Salvia miltiorrhiza and is used to treat vascular diseases. To better understand its mechanism, the antioxidant capacities of Sal B was ... Salvianolic acid B(Sal B) is an active component of traditional Chinese medicine Salvia miltiorrhiza and is used to treat vascular diseases. To better understand its mechanism, the antioxidant capacities of Sal B was evaluated with human endothelial cells under oxidative stress. Human endothelial cells were pretreated with Sal B for 12 h followed by hydrogen peroxide for another 12 h. Production of reactive oxygen species (ROS), activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX), and concentration of glu-tathione were measured. Protective effect of Sal B on the endothelial cells from hydrogen peroxide-induced damage was observed, and ROS production in the cells was found significantly inhibited. Sal B remarkably enhanced the activities of antioxidant enzymes SOD, CAT and GPX. Furthermore, Sal B up-regulated the intracellular glu-tathione concentration. The results indicate that Sal B protected endothelial cells from oxidative stress by improving the redox status of the cells through enhancing the antioxidant enzyme activities and increasing the reductive glu-tathione concentration after the oxidative challenge. 展开更多
关键词 salvianolic acid B redox status human endothelial cell hydrogen peroxide oxidative stress antioxidant enzyme reductive glutathione
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Effect of ligand troglitazone on peroxisome proliferator-activated receptor γ expression and cellular growth in human colon cancer cells 被引量:2
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作者 Mei Ming Jie-Ping Yu +3 位作者 Xiang-Zhi Meng Yan-Hong Zhou Hong-Gang Yu He-Sheng kuo 《World Journal of Gastroenterology》 SCIE CAS CSCD 2006年第45期7263-7270,共8页
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 mole... 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. 展开更多
关键词 Peroxisome proliferator-activated receptor γ Colon cancer TROGLITAZONE Cellular growth Cell cycle APOPTOSIS
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Antioxidative capacity and enzyme activity in Haematococcus pluvialis cells exposed to superoxide free radicals 被引量:5
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作者 刘建国 张晓丽 +1 位作者 孙延红 林伟 《Chinese Journal of Oceanology and Limnology》 SCIE CAS CSCD 2010年第1期1-9,共9页
The antioxidative capacity of astaxanthin and enzyme activity of reactive oxygen eliminating enzymes such as superoxide dismutase (SOD),peroxidase (POD),catalase (CAT) and ascorbate peroxidase (APX) were studied in th... The antioxidative capacity of astaxanthin and enzyme activity of reactive oxygen eliminating enzymes such as superoxide dismutase (SOD),peroxidase (POD),catalase (CAT) and ascorbate peroxidase (APX) were studied in three cell types of Haematococcus pluvialis exposed to high concentrations of a superoxide anion radical (O2ˉ).The results show that defensive enzymes and astaxanthin-related mechanisms were both active in H.pluvialis during exposure to reactive oxygen species (ROS) such as Oˉ2.Astaxanthin reacted with ROS much faster than did the protective enzymes,and had the strongest antioxidative capacity to protect against lipid peroxidation.The defensive mechanisms varied significantly between the three cell types and were related to the level of astaxanthin that had accumulated in those cells.Astaxanthin-enriched red cells had the strongest antioxidative capacity,followed by brown cells,and astaxanthin-deficient green cells.Although there was no significant increase in expression of protective enzymes,the malondialdehyde (MDA) content in red cells was sustained at a low level because of the antioxidative effect of astaxanthin,which quenched Oˉ2 before the protective enzymes could act.In green cells,astaxanthin is very low or absent;therefore,scavenging of ROS is inevitably reliant on antioxidative enzymes.Accordingly,in green cells,these enzymes play the leading role in scavenging ROS,and the expression of these enzymes is rapidly increased to reduce excessive ROS.However,because ROS were constantly increased in this study,the enhance enzyme activity in the green cells was not able to repair the ROS damage,leading to elevated MDA content.Of the four defensive enzymes measured in astaxanthin-deficient green cells,SOD eliminates Oˉ2,POD eliminates H2O2,which is a by-product of SOD activity,and APX and CAT are then initiated to scavenge excessive ROS. 展开更多
关键词 ASTAXANTHIN Haematococcus pluvialis lipid peroxidation reactive oxygen species (ROS)
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Preliminary Study of Oxidative Stress in Human Hepatocellular Carcinoma and Adjacent Normal Liver Tissues
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作者 Hongwei Yu Chunying Chen +5 位作者 Jiangxue Wang Yuxi Gao Guilong Deng Yingbin Liu Shuyou Peng Zhifang Chai 《Chinese Journal of Clinical Oncology》 CSCD 2006年第1期11-14,共4页
OBJECTIVE The antioxidative system in human hepatocellular carcinoma was investigated. METHODS The activities of cytosolic catalase (CAT), superoxide dismu-tase, glutathione peroxidase (GSH-Px), glutathione S-tranfera... OBJECTIVE The antioxidative system in human hepatocellular carcinoma was investigated. METHODS The activities of cytosolic catalase (CAT), superoxide dismu-tase, glutathione peroxidase (GSH-Px), glutathione S-tranferase and levels of reduced glutathione, total protein thiols and malondialdehyde were assayed in 10 cases of hepatocellular carcinoma and adjacent normal liver. RESULTS Hepatoma tissues showed higher activities of CAT, GSH -Px and lower content of total antioxidative capacity compared to adjacent normal liver tissue (P<0.05). CONCLUSION These findings suggest that the antioxidative defense-related enzymes and antioxidants are largely regulated in hepatoma cells. However, the mechanism which is not clear requires further investigation. 展开更多
关键词 human hepatocellular carcinoma antioxidative enzymes oxidative stress.
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