12 results on '"Ze, Yuguan"'
Search Results
2. Toxic effects of TiO2 nanoparticles in primary cultured rat sertoli cells are mediated via a dysregulated Ca2+ /PKC/p38 MAPK/NF-κB cascade
- Author
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Ye, Lingqun, primary, Hong, Fashui, additional, Ze, Xiao, additional, Li, Lingjuan, additional, Zhou, Yaoming, additional, and Ze, Yuguan, additional
- Published
- 2017
- Full Text
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3. TiO2 nanoparticles‐induced apoptosis of primary cultured Sertoli cells of mice
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Hong, Fashui, primary, Zhao, Xiaoyang, additional, Chen, Ming, additional, Zhou, Yingjun, additional, Ze, Yuguan, additional, Wang, Ling, additional, Wang, Yajing, additional, Ge, Yushuang, additional, Zhang, Qi, additional, and Ye, Lingqun, additional
- Published
- 2015
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4. Mechanisms of TiO2nanoparticle-induced neuronal apoptosis in rat primary cultured hippocampal neurons
- Author
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Sheng, Lei, primary, Ze, Yuguan, additional, Wang, Ling, additional, Yu, Xiaohong, additional, Hong, Jie, additional, Zhao, Xiaoyang, additional, Ze, Xiao, additional, Liu, Dong, additional, Xu, Bingqing, additional, Zhu, Yunting, additional, Long, Yi, additional, Lin, Anan, additional, Zhang, Chi, additional, Zhao, Yue, additional, and Hong, Fashui, additional
- Published
- 2014
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5. Neurotoxicity and gene-expressed profile in brain-injured mice caused by exposure to titanium dioxide nanoparticles
- Author
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Ze, Yuguan, primary, Hu, Renping, additional, Wang, Xiaochun, additional, Sang, Xuezi, additional, Ze, Xiao, additional, Li, Bi, additional, Su, Junju, additional, Wang, Yuan, additional, Guan, Ning, additional, Zhao, Xiaoyang, additional, Gui, Suxin, additional, Zhu, Liyuan, additional, Cheng, Zhe, additional, Cheng, Jie, additional, Sheng, Lei, additional, Sun, Qingqing, additional, Wang, Ling, additional, and Hong, Fashui, additional
- Published
- 2013
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6. Cardiac oxidative damage in mice following exposure to nanoparticulate titanium dioxide
- Author
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Sheng, Lei, primary, Wang, Xiaochun, additional, Sang, Xuezi, additional, Ze, Yuguan, additional, Zhao, Xiaoyang, additional, Liu, Dong, additional, Gui, Suxin, additional, Sun, Qingqing, additional, Cheng, Jie, additional, Cheng, Zhe, additional, Hu, Renping, additional, Wang, Ling, additional, and Hong, Fashui, additional
- Published
- 2013
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7. Nanoparticulate TiO 2 -mediated inhibition of the Wnt signaling pathway causes dendritic development disorder in cultured rat hippocampal neurons.
- Author
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Hong F, Ze Y, Zhou Y, Hong J, Yu X, Sheng L, and Wang L
- Subjects
- Animals, Cells, Cultured, Dendrites metabolism, Dendrites pathology, Hippocampus cytology, Hippocampus metabolism, Hippocampus pathology, Neurogenesis, Neurons cytology, Neurons metabolism, Rats, Rats, Sprague-Dawley, Nanoparticles adverse effects, Neurons pathology, Titanium adverse effects, Wnt Signaling Pathway
- Abstract
Titanium dioxide nanoparticles (TiO
2 NPs) are increasingly used in daily life, in industry, and in environmental clearing, but their potential neurodevelopmental toxicity has been highly debated. In this study, we explored whether TiO2 NPs inhibited development of dendritic morphology and identified possible molecular mechanisms associated with this inhibition in primary cultured rat hippocampal neurons. Results showed that TiO2 NPs decreased neurite length, the number of branches and the spine density, and impaired mitochondrial function in the developing neurons. Furthermore, TiO2 NPs significantly reduced the expression of several proteins involved in canonical Wnt3a/β-catenin signaling including Wnt3a, β-catenin, p-GSK-3β, and CyclinD1 and conversely, elevated GSK-3β expression. In addition to altering expression of proteins involved in canonical Wnt3a/β-catenin signaling, TiO2 NPs decreased expression of proteins invovled in non-canonical Wnt signaling, including, MKLP1, CRMP3, ErbB4, and KIF17. Taken together, these results indicate that suppression of dendritic development caused by TiO2 NPs is associated with inhibition of activation of the Wnt/β-catenin pathway or non-canonical Wnt pathway-induced expression of microtubule cytoskeletal components in the developing neurons. © 2017 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 105A: 2139-2149, 2017., (© 2017 Wiley Periodicals, Inc.)- Published
- 2017
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- View/download PDF
8. Toxic effects of TiO 2 nanoparticles in primary cultured rat sertoli cells are mediated via a dysregulated Ca 2+ /PKC/p38 MAPK/NF-κB cascade.
- Author
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Ye L, Hong F, Ze X, Li L, Zhou Y, and Ze Y
- Subjects
- Animals, Calcium immunology, Calcium Signaling immunology, MAP Kinase Signaling System immunology, Male, NF-kappa B metabolism, Protein Kinase C metabolism, Rats, Rats, Sprague-Dawley, Sertoli Cells pathology, Calcium Signaling drug effects, MAP Kinase Signaling System drug effects, NF-kappa B immunology, Protein Kinase C immunology, Sertoli Cells immunology, Titanium toxicity, p38 Mitogen-Activated Protein Kinases metabolism
- Abstract
Although numerous studies have demonstrated that titanium dioxide nanoparticles (TiO
2 NPs) can be accumulated in various animal organs and can cause toxicity, there is currently only limited data regarding reproductive toxicity especially on the toxic mechanisms of TiO2 NPs in Sertoli cells. In order to investigate the mechanism of reproductive toxicity, primary cultured rat Sertoli cells were exposed to 5, 15, or 30 μg/mL TiO2 NPs for 24 h, and TiO2 NPs internalization, expression of PKC (p-PKC) and p38 MAPK (p-p38 MAPK) as well as calcium homeostasis were examined. Our findings demonstrated that TiO2 NPs crossed the membrane into the cytoplasm or nucleus, and significantly suppressed cell viability of primary cultured rat Sertoli cells in a concentration-dependent manner. Furthermore, immunological dysfunction caused by TiO2 NPs was involved in the increased expression of NF-κB, TNF-α, and IL-1β, and decreased IκB expression. TiO2 NPs significantly decreased Ca2+ -ATPase and Ca2+ /Mg2+ -ATPase activity and enhanced intracellular Ca2+ levels, and up-regulated the expression of p-PKC and p-p38 MAPK in a dose-dependent manner in primary cultured rat Sertoli cells. Taken together, these findings indicate that TiO2 NPs may induce immunological dysfunction of primary cultured rat Sertoli cells by stimulating the Ca2+ /PKC/p38 MAPK cascade, which triggers NF-κB activation and ultimately induces the expression of inflammatory cytokines in primary cultured rat Sertoli cells. © 2017 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 105A: 1374-1382, 2017., (© 2017 Wiley Periodicals, Inc.)- Published
- 2017
- Full Text
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9. TiO2 nanoparticles-induced apoptosis of primary cultured Sertoli cells of mice.
- Author
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Hong F, Zhao X, Chen M, Zhou Y, Ze Y, Wang L, Wang Y, Ge Y, Zhang Q, and Ye L
- Subjects
- Animals, Antioxidants metabolism, Cell Survival drug effects, Cells, Cultured, Cytokines metabolism, Hydrodynamics, L-Lactate Dehydrogenase metabolism, Lipid Peroxidation drug effects, Male, Membrane Potential, Mitochondrial drug effects, Metal Nanoparticles chemistry, Metal Nanoparticles ultrastructure, Mice, Inbred ICR, Reactive Oxygen Species metabolism, Sertoli Cells metabolism, Sertoli Cells ultrastructure, X-Ray Diffraction, Apoptosis drug effects, Metal Nanoparticles toxicity, Sertoli Cells cytology, Titanium toxicity
- Abstract
Titanium dioxide nanoparticles (TiO2 NPs), as largest production and use of nanomaterials, have been demonstrated to have a potential toxicity on reproductive system. However, the mechanism underlying male reproductive toxicity of TiO2 NPs remains limited. Thus, our study was designed to examine the cellular viability, apoptosis, oxidative stress, antioxidant capacity, and expression of apoptotic cytokines in primary cultured Sertoli cells isolated from mice under TiO2 NPs exposure. Results showed that TiO2 NPs exposure from 5 to 30 μg/mL resulted in reduction of cell viability, lactate dehydrogenase release, and induction of apoptosis or death on Sertoli cells. TiO2 NPs could migrate to Sertoli cells, which induced mitochondria-mediated or endoplasmic-reticulum-mediated apoptotic changes including elevation in reactive oxygen species (ROS) generation and reductions in superoxide dismutase, catalase, and glutathione peroxidase activities, decreases in mitochondrial membrane potential (ΔΨm), and releases of cytochrome c into the cytosol. In addition, upregulation of cytochrome c, Bax, caspase-3, glucose-regulated protein 78, and C/EBP homologous protein and caspase-12 protein expression, and downregulation of bcl-2 protein expression in primary cultured Sertoli cells induced by TiO2 NPs treatment. All of the results suggested that ROS generation may play a critical role in the initiation of TiO2 NPs-induced apoptosis by mediation of the disruption of ΔΨm, the cytochrome c release, and further the activation of caspase cascade and unfolded protein response signaling pathway., (© 2015 Wiley Periodicals, Inc.)
- Published
- 2016
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10. Mechanisms of TiO2 nanoparticle-induced neuronal apoptosis in rat primary cultured hippocampal neurons.
- Author
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Sheng L, Ze Y, Wang L, Yu X, Hong J, Zhao X, Ze X, Liu D, Xu B, Zhu Y, Long Y, Lin A, Zhang C, Zhao Y, and Hong F
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- Animals, Apoptosis Regulatory Proteins biosynthesis, Cell Survival drug effects, Cells, Cultured, Hippocampus pathology, Membrane Potential, Mitochondrial drug effects, Nanoparticles chemistry, Neurons pathology, Rats, Rats, Sprague-Dawley, Apoptosis drug effects, Hippocampus metabolism, Nanoparticles adverse effects, Neurons metabolism, Signal Transduction drug effects, Titanium toxicity
- Abstract
Exposure to titanium dioxide nanoparticles (TiO2 NPs) has been demonstrated to decrease learning and memory of animals. However, whether the impacts of these NPs on the recognition function are involved in hippocamal neuron damages is poorly understood. In this study, primary cultured hippocampal neurons from one-day-old fetal Sprague-Dawley rats were exposed to 5, 15, or 30 µg/mL TiO2 NPs for 24 h, we investigated cell viability, ultrastructure, and mitochondrial membrane potential (MMP), calcium homeostasis, oxidative stress, antioxidant capacity, apoptotic signaling pathway associated with the primary cultured hippocamal neuron apoptosis. Our findings showed that TiO2 NP treatment resulted in reduction of cell viability, promoted lactate dehydrogenase release, apoptosis, and increased neuron apoptotic rate in a dose-dependent manner. Furthermore, TiO2 NPs led to [Ca(2+)]i elevation, and MMP reduction, up-regulated protein expression of cytochrome c, Bax, caspase-3, glucose-regulated protein 78, C/EBP homologous protein and caspase-12, and down-regulated bcl-2 expression in the primary cultured hippocampal neurons. These findings suggested that hippocampal neuron apoptosis caused by TiO2 NPs may be associated with mitochondria-mediated signal pathway and endoplasmic reticulum-mediated signal pathway., (© 2014 Wiley Periodicals, Inc.)
- Published
- 2015
- Full Text
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11. Immunomodulatory effects in the spleen-injured mice following exposure to titanium dioxide nanoparticles.
- Author
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Sang X, Fei M, Sheng L, Zhao X, Yu X, Hong J, Ze Y, Gui S, Sun Q, Ze X, Wang L, and Hong F
- Subjects
- Animals, Apoptosis drug effects, Body Weight drug effects, Chemokines metabolism, Enzyme-Linked Immunosorbent Assay, Female, Gene Expression Regulation drug effects, Inflammation Mediators metabolism, Mice, Organ Specificity drug effects, RNA, Messenger genetics, RNA, Messenger metabolism, Real-Time Polymerase Chain Reaction, Spleen drug effects, Spleen pathology, Titanium administration & dosage, Immunologic Factors pharmacology, Nanoparticles chemistry, Spleen immunology, Spleen injuries, Titanium pharmacology
- Abstract
Immune injuries following the exposure of titanium dioxide nanoparticles (TiO₂ NPs) have been greatly concerned along with the TiO₂ NPs are widely used in pharmacology and daily life. However, very little is known about the immunomodulatory mechanisms in the spleen-injured mice due to TiO₂ NPs exposure. In this study, mice were continuously exposed to 2.5, 5, or 10 TiO₂ NPs mg kg(-1) body weight for 90 days with intragastric administration to investigate the immunomodulatory mechanisms in the spleen. The findings showed that TiO₂ NPs exposure resulted in significant increases in spleen and thymus indices, and titanium accumulation, in turn led to histopathological changes and splenocyte apoptosis. Furthermore, the exposure of TiO₂ NPs could significantly increase the levels of macrophage inflammatory protein (MIP)-1α, MIP-2, Eotaxin, monocyte chemotactic protein-1, interferon-γ, vascular cell adhesion molecule-1, interleukin-13, interferon-γ-inducible protein-10, migration inhibitory factor, CD69, major histocompatibility complex, protein tyrosine phosphatase, protein tyrosine kinase 1, basic fibroblast growth factor, Fasl, and GzmB expression, whereas markedly decrease the levels of NKG2D, NKp46, 2B4 expression involved in immune responses, lymphocyte healing and apoptosis. These findings would better understand toxicological effects induced by TiO₂ NPs exposure., (© 2013 Wiley Periodicals, Inc.)
- Published
- 2014
- Full Text
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12. Neurotoxicity and gene-expressed profile in brain-injured mice caused by exposure to titanium dioxide nanoparticles.
- Author
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Ze Y, Hu R, Wang X, Sang X, Ze X, Li B, Su J, Wang Y, Guan N, Zhao X, Gui S, Zhu L, Cheng Z, Cheng J, Sheng L, Sun Q, Wang L, and Hong F
- Subjects
- Animals, Behavior, Animal drug effects, Brain metabolism, Brain pathology, Brain Injuries chemically induced, Brain Injuries pathology, Cell Proliferation drug effects, Female, Gene Expression Profiling, Humans, Mice, Mice, Inbred ICR, Nanoparticles administration & dosage, Neuroglia metabolism, Neuroglia pathology, Neurotoxicity Syndromes pathology, Oxidative Stress drug effects, Sunscreening Agents pharmacology, Titanium pharmacology, Brain Injuries metabolism, Gene Expression Regulation drug effects, Nanoparticles adverse effects, Nerve Tissue Proteins biosynthesis, Neurotoxicity Syndromes metabolism, Sunscreening Agents adverse effects, Titanium adverse effects
- Abstract
Titanium dioxide nanoparticles (TiO2 NPs) are widely used in toothpastes, sunscreens, and products for cosmetic purpose that the human use daily. Although the neurotoxicity induced by TiO2 NPs has been demonstrated, very little is known about the molecular mechanisms underlying the brain cognition and behavioral injury. In this study, mice were exposed to 2.5, 5, and 10 mg/kg body weight (BW) TiO2 NPs by nasal administration for 90 consecutive days, respectively, and their brains' injuries and brain gene-expressed profile were investigated. Our findings showed that TiO2 NPs could be translocated and accumulated in brain, led to oxidative stress, overproliferation of all glial cells, tissue necrosis as well as hippocampal cell apoptosis. Furthermore, microarray data showed significant alterations in the expression of 249 known function genes, including 113 genes upregulation and 136 genes downregulation following exposure to 10 mg/kg BW TiO2 NPs, which were associated with oxidative stress, immune response, apoptosis, memory and learning, brain development, signal transduction, metabolic process, DNA repair, response to stimulus, and cellular process. Especially, significant increases in Col1a1, serine/threonine-protein kinase 1, Ctnnb1, cysteine-serine-rich nuclear protein-1, Ddit4, Cyp2e1, and Krev interaction trapped protein 1 (Krit1) expressions and great decreases in DA receptor D2, Neu1, Fc receptor-like molecules, and Dhcr7 expressions following long-term exposure to TiO2 NPs resulted in neurogenic disease states in mice. Therefore, these genes may be potential biomarkers of brain toxicity caused by TiO2 NPs exposure, and the application of TiO2 NPs should be carried out cautiously., (© 2013 Society of Plastics Engineers.)
- Published
- 2014
- Full Text
- View/download PDF
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