The Experts below are selected from a list of 249 Experts worldwide ranked by ideXlab platform
Minmin Tian - One of the best experts on this subject based on the ideXlab platform.
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Nano-selenium attenuates nickel-induced Testosterone Synthesis disturbance through inhibition of MAPK pathways in Sprague-Dawley rats
Environmental toxicology, 2019Co-Authors: Xiaoqin Gan, Aijie Han, Xiaotian Zhang, Minmin Tian, Qiannan E, Qiong Zhang, Yunyu Cai, Caixia WangAbstract:The aim of this study was to investigate the protective effects of Nano-Se against Ni-induced Testosterone Synthesis disorder in rats and determine the underlying protective mechanism. Sprague-Dawley rats were co-treated with Ni (5.0 mg/kg, i.p.) and Nano-Se (0.5, 1.0, and 2.0 mg/kg, oral gavage) for 14 days after which various endpoints were evaluated. The Ni-induced abnormal pathological changes and elevated 8-OHdG levels in the testes were attenuated by Nano-Se administration. Importantly, decreased serum Testosterone levels in the Ni-treated rats were significantly restored by Nano-Se treatment, particularly at 1.0 and 2.0 mg/kg. Furthermore, the mRNA and protein levels of Testosterone synthetase were increased by Nano-Se compared to the Ni group, whereas phosphorylated protein expression levels of mitogen-activated protein kinase (MAPK) pathways were suppressed by Nano-Se administration in the Ni-treated rats. Overall, the results suggest that Nano-Se may ameliorate the Ni-induced Testosterone Synthesis disturbance via the inhibition of ERK1/2, p38, and JNK MAPK pathways.
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ROS generation and MAPKs activation contribute to the Ni-induced Testosterone Synthesis disturbance in rat Leydig cells
Toxicology letters, 2018Co-Authors: Aijie Han, Lingyue Zou, Xiaoqin Gan, Fangfang Liu, Xuhong Chang, Xiaotian Zhang, Minmin TianAbstract:Nickel (Ni) can disorder Testosterone Synthesis in rat Leydig cells, whereas the mechanisms remain unclear. The aim of this study was to investigate the role of reactive oxygen species (ROS) and mitogen-activated protein kinases (MAPKs) in Ni-induced disturbance of Testosterone Synthesis in rat Leydig cells. The Testosterone production and ROS levels were detected in Leydig cells. The mRNA and protein levels of Testosterone synthetase, including StAR, CYP11A1, 3β-HSD, CYP17A1 and 17β-HSD, were determined. Effects of Ni on the ERK1/2, p38 and JNK MAPKs were also investigated. The results showed that Ni triggered ROS generation, consequently resulted in the decrease of Testosterone synthetase expression and Testosterone production in Leydig cells, which were then attenuated by ROS scavengers of N-acetylcysteine (NAC) and 2,2,6,6-tetramethyl-1-piperidinyloxy (TEMPO), indicating that ROS are involved in the Ni-induced Testosterone bioSynthesis disturbance. Meanwhile Ni activated the ERK1/2, p38 and JNK MAPKs. Furthermore, Ni-inhibited Testosterone synthetase expression levels and Testosterone secretion were all alleviated by co-treatment with MAPK specific inhibitors (U0126 and SB203580, respectively), implying that Ni inhibited Testosterone Synthesis through activating ERK1/2 and p38 MAPK signal pathways in Leydig cells. In conclusion, these findings suggest that Ni causes Testosterone Synthesis disorder, partly, via ROS and MAPK signal pathways.
B Qiao - One of the best experts on this subject based on the ideXlab platform.
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effects of wnt β catenin signaling pathway and star d7 on Testosterone Synthesis
Acta Endocrinologica-bucharest, 2018Co-Authors: Tianbiao Zhang, Tao Zheng, Chao Liang Wang, Weidong Zhang, Donghui Jia, Rui Wang, B QiaoAbstract:Background This study aimed to assess the mechanism through which Wnt/ beta - catenin signaling pathway, and StarD7, prometes Testosterone Synthesis, and to explore a new pathway for the regulation of Testosterone Synthesis. Animals and methods Leydig cells were isolated from male Sprague-Dawley rats divided into four groups and treated with Annexin 5 in concentration of 0, 0.1, 1 and 10 nmol/L. Testosterone secretion, expression of StarD7, StarD7 mRNA, β-catenin and changes of β - catenin localization in Leydig cells of testis of rats were tested in the four groups. Results mRNA and protein levels of StarD7 and β-catenin increased significantly, upon stimulation with 1 nmol/L annexin 5. Accumulation of β-catenin inside the cells and the nucleus, was observed by immunofluorescence staining, in cells treated with annexin 5. These findings indicate a possible role of StarD7 and β-catenin in the process of annexin5-mediated stimulation of Testosterone Synthesis. Conclusions Wnt/β-catenin signaling pathway and StarD7 are involved in the process of annexin5 stimulation of Testosterone Synthesis. Activation of Wnt/ β-catenin signaling pathway by Annexin5, and increase in StarD7 expression lead to elevated expression of key regulatory enzymes in Testosterone Synthesis, thus promoting Testosterone Synthesis.
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EFFECTS OF Wnt / β-CATENIN SIGNALING PATHWAY AND STAR D7 ON Testosterone Synthesis.
Acta endocrinologica (Bucharest Romania : 2005), 2018Co-Authors: Tianbiao Zhang, Tao Zheng, Chao Liang Wang, Weidong Zhang, Donghui Jia, Rui Wang, B QiaoAbstract:This study aimed to assess the mechanism through which Wnt/ beta - catenin signaling pathway, and StarD7, prometes Testosterone Synthesis, and to explore a new pathway for the regulation of Testosterone Synthesis. Leydig cells were isolated from male Sprague-Dawley rats divided into four groups and treated with Annexin 5 in concentration of 0, 0.1, 1 and 10 nmol/L. Testosterone secretion, expression of StarD7, StarD7 mRNA, β-catenin and changes of β - catenin localization in Leydig cells of testis of rats were tested in the four groups. mRNA and protein levels of StarD7 and β-catenin increased significantly, upon stimulation with 1 nmol/L annexin 5. Accumulation of β-catenin inside the cells and the nucleus, was observed by immunofluorescence staining, in cells treated with annexin 5. These findings indicate a possible role of StarD7 and β-catenin in the process of annexin5-mediated stimulation of Testosterone Synthesis. Wnt/β-catenin signaling pathway and StarD7 are involved in the process of annexin5 stimulation of Testosterone Synthesis. Activation of Wnt/ β-catenin signaling pathway by Annexin5, and increase in StarD7 expression lead to elevated expression of key regulatory enzymes in Testosterone Synthesis, thus promoting Testosterone Synthesis.
Yaoyao Xiao - One of the best experts on this subject based on the ideXlab platform.
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Zearalenone perturbs the circadian clock and inhibits Testosterone Synthesis in mouse Leydig cells.
Journal of toxicology and environmental health. Part A, 2020Co-Authors: Lijia Zhao, Yaoyao Xiao, Jing Zhang, Yaojia Zhang, Luda Yang, Xiaoyu Wang, Haizhen JiangAbstract:Zearalenone (ZEA), a mycotoxin, is known to impair reproductive capability by disrupting the Synthesis and secretion of Testosterone by Leydig cells (LCs), although the mechanism is unknown. Robust rhythmicity of circadian clock and steroidogenic genes were identified in LCs. The aim of this study was to examine whether ZEA significantly attenuated the transcription of core clock genes (Bmal1, Dbp, Per2, and Nr1d1) as well as steroidogenic genes (StAR, Hsd3b2, and Cyp11a1) in mouse testis Leydig cell line (TM3). Western blotting confirmed declines in BMAL1, NR1D1, and StAR protein levels. ZEA also suppressed secreted Testosterone levels. In primary LCs, isolated from PER2::LUCIFERASE reporter gene knock in mice, ZEA diminished the amplitude of PER2::LUC expression, and induced a phase shift and period extension. In primary LCs, ZEA also suppressed the expression levels of core clock and steroidogenic genes, reduced protein levels of BMAL1, and decreased Testosterone secretion. In vivo expression of core clock and steroidogenic genes were reduced in testes of mice exposed to ZEA for 1 week leading to decreased serum Testosterone levels. In summary, data suggest that ZEA may impair Testosterone Synthesis through attenuation of the circadian clock in LCs culminating in reproductive dysfunction in male mammals .
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Bisphenol A attenuates Testosterone production in Leydig cells via the inhibition of NR1D1 signaling.
Chemosphere, 2020Co-Authors: Linlin Zhang, Luda Yang, Xiaoyu Wang, Lei Gao, Zhaoxia Pang, Qiyang Yao, Yaoyao XiaoAbstract:Bisphenol A (BPA) is an endocrine-disrupting compound that impairs Testosterone Synthesis in male mammals. A circadian clock gene deficiency leads to diminished fertility and even infertility in male mice. However, whether circadian clock signaling pathways mediate the suppressive effect of BPA on Testosterone Synthesis in Leydig cells (LCs) remains unknown. The present study aims to detect the effect of BPA on cellular circadian clock and Testosterone Synthesis in mouse LCs, and examine the mechanisms underlying NR1D1 signaling. BPA treatment significantly attenuated the transcription levels of Nr1d1 and steroidogenic genes (Hsd3b2 and Hsd17b3) in TM3 cells, but increased other circadian clock gene levels (Per2 and Dbp). BPA treatment also significantly downregulated NR1D1 and StAR protein expression, but upregulated BMAL1 protein expression in TM3 cells. Furthermore, there was a marked decline in Testosterone production in BPA-treated TM3 cells. Intraperitoneal injection of BPA profoundly reduced NR1D1 and StAR protein levels and steroidogenic gene transcription levels (Cyp11a1, Hsd3b2, and Hsd17b3), while enhancing BMAL1 protein and other circadian clock gene (Per2 and Dbp) levels in mouse testes. Notably, serum Testosterone levels were also drastically reduced in BPA-treated mice. Moreover, SR9009, an NR1D1 agonist, augmented Testosterone production in TM3 cells via elevated expression of steroidogenic genes (StAR, Cyp11a1 and Hsd17b3). Conversely, Nr1d1 knockdown inhibited Testosterone accumulation and attenuated steroidogenic gene expression. Moreover, treatment with SR9009 partially reversed the BPA effect on the circadian clock and Testosterone production. Taken together, our study demonstrates that BPA perturbs Testosterone production, at least partially, via inhibiting NR1D1 signaling in LCs.
Xiaoqin Gan - One of the best experts on this subject based on the ideXlab platform.
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Nano-selenium attenuates nickel-induced Testosterone Synthesis disturbance through inhibition of MAPK pathways in Sprague-Dawley rats
Environmental toxicology, 2019Co-Authors: Xiaoqin Gan, Aijie Han, Xiaotian Zhang, Minmin Tian, Qiannan E, Qiong Zhang, Yunyu Cai, Caixia WangAbstract:The aim of this study was to investigate the protective effects of Nano-Se against Ni-induced Testosterone Synthesis disorder in rats and determine the underlying protective mechanism. Sprague-Dawley rats were co-treated with Ni (5.0 mg/kg, i.p.) and Nano-Se (0.5, 1.0, and 2.0 mg/kg, oral gavage) for 14 days after which various endpoints were evaluated. The Ni-induced abnormal pathological changes and elevated 8-OHdG levels in the testes were attenuated by Nano-Se administration. Importantly, decreased serum Testosterone levels in the Ni-treated rats were significantly restored by Nano-Se treatment, particularly at 1.0 and 2.0 mg/kg. Furthermore, the mRNA and protein levels of Testosterone synthetase were increased by Nano-Se compared to the Ni group, whereas phosphorylated protein expression levels of mitogen-activated protein kinase (MAPK) pathways were suppressed by Nano-Se administration in the Ni-treated rats. Overall, the results suggest that Nano-Se may ameliorate the Ni-induced Testosterone Synthesis disturbance via the inhibition of ERK1/2, p38, and JNK MAPK pathways.
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ROS generation and MAPKs activation contribute to the Ni-induced Testosterone Synthesis disturbance in rat Leydig cells
Toxicology letters, 2018Co-Authors: Aijie Han, Lingyue Zou, Xiaoqin Gan, Fangfang Liu, Xuhong Chang, Xiaotian Zhang, Minmin TianAbstract:Nickel (Ni) can disorder Testosterone Synthesis in rat Leydig cells, whereas the mechanisms remain unclear. The aim of this study was to investigate the role of reactive oxygen species (ROS) and mitogen-activated protein kinases (MAPKs) in Ni-induced disturbance of Testosterone Synthesis in rat Leydig cells. The Testosterone production and ROS levels were detected in Leydig cells. The mRNA and protein levels of Testosterone synthetase, including StAR, CYP11A1, 3β-HSD, CYP17A1 and 17β-HSD, were determined. Effects of Ni on the ERK1/2, p38 and JNK MAPKs were also investigated. The results showed that Ni triggered ROS generation, consequently resulted in the decrease of Testosterone synthetase expression and Testosterone production in Leydig cells, which were then attenuated by ROS scavengers of N-acetylcysteine (NAC) and 2,2,6,6-tetramethyl-1-piperidinyloxy (TEMPO), indicating that ROS are involved in the Ni-induced Testosterone bioSynthesis disturbance. Meanwhile Ni activated the ERK1/2, p38 and JNK MAPKs. Furthermore, Ni-inhibited Testosterone synthetase expression levels and Testosterone secretion were all alleviated by co-treatment with MAPK specific inhibitors (U0126 and SB203580, respectively), implying that Ni inhibited Testosterone Synthesis through activating ERK1/2 and p38 MAPK signal pathways in Leydig cells. In conclusion, these findings suggest that Ni causes Testosterone Synthesis disorder, partly, via ROS and MAPK signal pathways.
Aijie Han - One of the best experts on this subject based on the ideXlab platform.
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Nano-selenium attenuates nickel-induced Testosterone Synthesis disturbance through inhibition of MAPK pathways in Sprague-Dawley rats
Environmental toxicology, 2019Co-Authors: Xiaoqin Gan, Aijie Han, Xiaotian Zhang, Minmin Tian, Qiannan E, Qiong Zhang, Yunyu Cai, Caixia WangAbstract:The aim of this study was to investigate the protective effects of Nano-Se against Ni-induced Testosterone Synthesis disorder in rats and determine the underlying protective mechanism. Sprague-Dawley rats were co-treated with Ni (5.0 mg/kg, i.p.) and Nano-Se (0.5, 1.0, and 2.0 mg/kg, oral gavage) for 14 days after which various endpoints were evaluated. The Ni-induced abnormal pathological changes and elevated 8-OHdG levels in the testes were attenuated by Nano-Se administration. Importantly, decreased serum Testosterone levels in the Ni-treated rats were significantly restored by Nano-Se treatment, particularly at 1.0 and 2.0 mg/kg. Furthermore, the mRNA and protein levels of Testosterone synthetase were increased by Nano-Se compared to the Ni group, whereas phosphorylated protein expression levels of mitogen-activated protein kinase (MAPK) pathways were suppressed by Nano-Se administration in the Ni-treated rats. Overall, the results suggest that Nano-Se may ameliorate the Ni-induced Testosterone Synthesis disturbance via the inhibition of ERK1/2, p38, and JNK MAPK pathways.
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ROS generation and MAPKs activation contribute to the Ni-induced Testosterone Synthesis disturbance in rat Leydig cells
Toxicology letters, 2018Co-Authors: Aijie Han, Lingyue Zou, Xiaoqin Gan, Fangfang Liu, Xuhong Chang, Xiaotian Zhang, Minmin TianAbstract:Nickel (Ni) can disorder Testosterone Synthesis in rat Leydig cells, whereas the mechanisms remain unclear. The aim of this study was to investigate the role of reactive oxygen species (ROS) and mitogen-activated protein kinases (MAPKs) in Ni-induced disturbance of Testosterone Synthesis in rat Leydig cells. The Testosterone production and ROS levels were detected in Leydig cells. The mRNA and protein levels of Testosterone synthetase, including StAR, CYP11A1, 3β-HSD, CYP17A1 and 17β-HSD, were determined. Effects of Ni on the ERK1/2, p38 and JNK MAPKs were also investigated. The results showed that Ni triggered ROS generation, consequently resulted in the decrease of Testosterone synthetase expression and Testosterone production in Leydig cells, which were then attenuated by ROS scavengers of N-acetylcysteine (NAC) and 2,2,6,6-tetramethyl-1-piperidinyloxy (TEMPO), indicating that ROS are involved in the Ni-induced Testosterone bioSynthesis disturbance. Meanwhile Ni activated the ERK1/2, p38 and JNK MAPKs. Furthermore, Ni-inhibited Testosterone synthetase expression levels and Testosterone secretion were all alleviated by co-treatment with MAPK specific inhibitors (U0126 and SB203580, respectively), implying that Ni inhibited Testosterone Synthesis through activating ERK1/2 and p38 MAPK signal pathways in Leydig cells. In conclusion, these findings suggest that Ni causes Testosterone Synthesis disorder, partly, via ROS and MAPK signal pathways.