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  • 1
    Online Resource
    Online Resource
    Role of the BDNF/TrkB/CREB signaling pathway in the cytotoxicity of bisphenol S in SK‐N‐SH cells
    Wiley ; 2021
    In:  Journal of Biochemical and Molecular Toxicology Vol. 35, No. 6 ( 2021-06), p. 1-11
    Details
    In: Journal of Biochemical and Molecular Toxicology, Wiley, Vol. 35, No. 6 ( 2021-06), p. 1-11
    Abstract: Bisphenol S (BPS) is associated with neurotoxicity, but its molecular mechanisms are unclear. Our aim was to investigate the role of the brain‐derived neurotrophic factor (BDNF)/tyrosine kinase B (TrkB)/cAMP‐response element‐binding protein (CREB) signaling pathway in BPS‐induced cytotoxicity in SK‐N‐SH cells. The cells were treated with various concentrations of BPS, and cell viability, apoptosis rate, mitochondrial membrane potential (MMP), and the BDNF, cleaved‐caspase‐3, B‐cell lymphoma 2 (Bcl‐2), Bcl‐2‐associated X protein (Bax), TrkB, CREB, and phospho‐CREB (p‐CREB) levels were determined. The effects of pretreatment with the TrkB activator 7,8‐dihydroxyflavone (7,8‐DHF) were also explored. BPS decreased SK‐N‐SH cell viability and altered their morphology. Their apoptosis rate was increased, as were the levels of the proapoptotic proteins Bax and cleaved‐caspase‐3, but MMP was decreased. Thus, BPS may induce mitochondria‐dependent apoptosis pathways. BPS also reduced the BDNF, TrkB, and p‐CREB levels, and pretreatment with 7,8‐DHF alleviated its cytotoxic effects. Thus, BPS‐induced cytotoxicity might be mediated by the BDNF/TrkB/CREB signaling pathway.
    Type of Medium: Online Resource
    ISSN: 1095-6670 , 1099-0461
    URL: Issue
    URL: Article
    DOI: 10.1002/jbt.v35.6
    DOI: 10.1002/jbt.22775
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 1481995-8
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Bisphenol S induces oxidative stress‐mediated impairment of testosterone synthesis by inhibiting the Nrf2/HO‐1 signaling pathway
    Wiley ; 2023
    In:  Journal of Biochemical and Molecular Toxicology Vol. 37, No. 3 ( 2023-03)
    Details
    In: Journal of Biochemical and Molecular Toxicology, Wiley, Vol. 37, No. 3 ( 2023-03)
    Abstract: Bisphenol S (BPS) is an environmental endocrine disruptor widely used in industrial production. BPS induces oxidative stress and exhibits male reproductive toxicity in mice, but the mechanisms by which BPS impairs steroid hormone synthesis are not fully understood. Nuclear factor erythroid 2‐related factor 2(Nrf2)/HO‐1 signaling is a key pathway in improving cellular antioxidant defense capacities. Therefore, this study explored the effects of exposure to BPS on testosterone synthesis in adult male mice and its mechanisms with regard to the Nrf2/HO‐1 signaling pathway. Adult male C57BL/6 mice were orally exposed to BPS (2, 20, and 200 mg/kg BW) with sesame oil as a vehicle (0.1 ml/10 g BW) per day for 28 consecutive days. The results showed that compared with the control group, serum testosterone levels were substantially reduced in the 20 and 200 mg/kg BPS treatment groups, and testicular testosterone levels were reduced in all BPS treatment groups. These changes were accompanied by a prominent decrease in the expression levels of testosterone synthesis‐related enzymes (STAR, CYP11A1, CYP17A1, HSD3B1, and HSD17B3) in the mouse testis. In addition, BPS induced oxidative stress in the testis by upregulating the messenger RNA and protein levels of Keap1 and downregulating the levels of Nrf2, HO‐1, and downstream antioxidant enzymes (CAT, SOD1, and Gpx4). In summary, our results indicate that exposure of adult male mice to BPS can inhibit Nrf2/HO‐1 signaling and antioxidant enzyme activity, which induces oxidative stress and thereby may impair testosterone synthesis in testicular tissues, leading to reproductive damage.
    Type of Medium: Online Resource
    ISSN: 1095-6670 , 1099-0461
    URL: Issue
    URL: Article
    DOI: 10.1002/jbt.v37.3
    DOI: 10.1002/jbt.23273
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 1481995-8
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    PFOS Disturbs BDNF-ERK-CREB Signalling in Association with Increased MicroRNA-22 in SH-SY5Y Cells
    Hindawi Limited ; 2015
    In:  BioMed Research International Vol. 2015 ( 2015), p. 1-10
    Details
    In: BioMed Research International, Hindawi Limited, Vol. 2015 ( 2015), p. 1-10
    Abstract: Perfluorooctane sulfonate (PFOS), a ubiquitous environmental pollutant, is neurotoxic to mammalian species. However, the underlying mechanism of its neurotoxicity was unclear. We hypothesized that PFOS suppresses BDNF expression to produce its neurotoxic effects by inhibiting the ERK-CREB pathway. SH-SY5Y human neuroblastoma cells were exposed to various concentrations of PFOS to examine the role of the BDNF-ERK-CREB signalling pathway in PFOS-induced apoptosis and cytotoxicity. Furthermore, to ascertain the mechanism by which PFOS reduces BDNF signalling, we examined the expression levels of miR-16 and miR-22, which potentially regulate BDNF mRNA translation at the posttranscriptional level. Results indicated that PFOS significantly decreased cell viability and induced apoptosis in SH-SY5Y cells. In addition, BDNF and pERK protein levels decreased after PFOS treatment; however, pCREB protein levels were significantly elevated in PFOS treated groups. TrkB protein expression increased in the 10  μ M and 50  μ M PFOS groups and significantly decreased in the 100  μ M PFOS group. Our results demonstrated that PFOS exposure decreased miR-16 expression and increased miR-22 expression, which may represent a possible mechanism by which PFOS decreases BDNF protein levels. PFOS may inhibit BDNF-ERK-CREB signalling by increasing miR-22 levels, which may, in part, explain the mechanism of PFOS neurotoxicity.
    Type of Medium: Online Resource
    ISSN: 2314-6133 , 2314-6141
    URL: Article
    DOI: 10.1155/2015/302653
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2015
    detail.hit.zdb_id: 2698540-8
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  • 4
    Online Resource
    Online Resource
    Puerarin Prevents Bisphenol S Induced Lipid Accumulation by Reducing Liver Lipid Synthesis and Promoting Lipid Metabolism in C57BL/6J Mice
    MDPI AG ; 2023
    In:  Toxics Vol. 11, No. 9 ( 2023-08-26), p. 736-
    Details
    In: Toxics, MDPI AG, Vol. 11, No. 9 ( 2023-08-26), p. 736-
    Abstract: Bisphenol S (BPS) is an environmental pollutant that can accumulate in the human body and cause harm. Puerarin (PUE) is a flavonoid with anti-inflammatory and antioxidant effects. In this study, we used 50 mg/kg/d BPS as a poison and PUE as an intervention for model mice for 42 d. BPS exposure significantly increased the levels of the impairment of the mice’s liver function, T-CHO, TG, LDL-C, ALT, and AST in the BPS group were significantly increased (p 〈 0.05). Additionally, BPS exposure caused inflammatory cell infiltration in the mice liver tissue and enhanced oxidative stress response, the level of MDA was significantly increased (p 〈 0.05). The expression of CD36 and pparγ was stimulated after BPS exposure. Moreover, the expression of cpt1a and cpt1b, which promote fatty acid oxidation, was downregulated. After PUE intervention, the levels of genes and proteins involved in lipid synthesis (PPARγ, SREBP1C, and FASN) and metabolism (Cpt1a, Cpt1b, and PPARα) in mice returned to those of the control group, or much higher than those in the BPS group. Therefore, we hypothesized that BPS causes lipid accumulation in the liver by promoting lipid synthesis and reducing lipid metabolism, whereas PUE reduces lipid synthesis and promotes lipid metabolism. Conclusively, our results imply that long-term exposure to BPS in mice affects liver lipid metabolism and that PUE intervention could maintain the liver function of mice at normal metabolic levels.
    Type of Medium: Online Resource
    ISSN: 2305-6304
    URL: Article
    DOI: 10.3390/toxics11090736
    Language: English
    Publisher: MDPI AG
    Publication Date: 2023
    detail.hit.zdb_id: 2733883-6
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  • 5
    Online Resource
    Online Resource
    Inflammation-like glial response in rat brain induced by prenatal PFOS exposure
    Elsevier BV ; 2011
    In:  NeuroToxicology Vol. 32, No. 1 ( 2011-01), p. 130-139
    Details
    In: NeuroToxicology, Elsevier BV, Vol. 32, No. 1 ( 2011-01), p. 130-139
    Type of Medium: Online Resource
    ISSN: 0161-813X
    URL: Article
    DOI: 10.1016/j.neuro.2010.10.001
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2011
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  • 6
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    Perfluorooctane Sulfonate Induces Apoptosis in N9 Microglial Cell Line
    SAGE Publications ; 2011
    In:  International Journal of Toxicology Vol. 30, No. 2 ( 2011-03), p. 207-215
    Details
    In: International Journal of Toxicology, SAGE Publications, Vol. 30, No. 2 ( 2011-03), p. 207-215
    Abstract: Perfluorooctane sulfonate (PFOS) is an environmental persistent acid found at low levels in human, wildlife, and environmental media samples. To study the apoptosis effects of PFOS on microglia, murine N9 cell line was used as a model in current research. The results showed that PFOS could reduce the cell viability significantly, and the cellular apoptosis induced by PFOS was closely accompanied with dissipation of mitochondria membrane potential, upregulation messenger RNAs (mRNAs) of p53, Bax, caspase 9, and caspase 3, and decreased expression of Bcl-2 mRNA. These results suggested that PFOS could disturb homeostasis of N9 cells, impact mitochondria, and affect gene expression of apoptotic regulators, all of which resulted in a start-up of apoptosis.
    Type of Medium: Online Resource
    ISSN: 1091-5818 , 1092-874X
    URL: Article
    DOI: 10.1177/1091581810387832
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2011
    detail.hit.zdb_id: 1500682-7
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  • 7
    Online Resource
    Online Resource
    NO-1886 ameliorates glycogen metabolism in insulin-resistant HepG2 cells by GSK-3 β signalling
    Oxford University Press (OUP) ; 2012
    In:  Journal of Pharmacy and Pharmacology Vol. 64, No. 2 ( 2012-01-04), p. 293-301
    Details
    In: Journal of Pharmacy and Pharmacology, Oxford University Press (OUP), Vol. 64, No. 2 ( 2012-01-04), p. 293-301
    Abstract: The aim of the study was to elucidate the possible role and mechanism of NO-1886 (ibrolipim, a lipoprotein lipase activator) in ameliorating insulin resistance induced by high palmitate. Methods HepG2 cells were cultured in RPMI 1640 medium and were treated with palmitate to induce insulin resistance. Free fatty acids (FFAs), glucose, glycogen, cell viability and mRNA and protein levels were analysed separately. Key findings We found that HepG2 cells treated with 0.5 mm palmitate for 48 h led to a significant decrease of insulin-induced glucose consumption (from 2.89 ± 0.85 mm in the control to 0.57 ± 0.44 mm in palmitate). Insulin resistance (IR) of HepG2 cells was induced by 0.5 mm palmitate for 48 h. NO-1886 stimulated glucose consumption, glycogen synthesis and FFA absorption in insulin-resistant HepG2 cells. Maximum stimulation effects were observed with 10 µm NO-1886 for 24 h. Compared with the dimethyl sulfoxide-treated group, 2.5 µm NO-1886 or higher could induce the mRNA expression of lipoprotein lipase. Meanwhile, NO-1886 increased the protein content of P-GSK-3βser9 and decreased the protein level of GSK-3β in insulin-resistant HepG2 cells, but NO-1886 didn't change the protein levels of PI3-Kp85 and Akt2. Conclusion Lipoprotein lipase activator NO-1886 could increase glycogen synthesis in HepG2 cells and could ameliorate the insulin resistance, which was associated with GSK-3 signalling.
    Type of Medium: Online Resource
    ISSN: 2042-7158 , 0022-3573
    URL: Article
    DOI: 10.1111/j.2042-7158.2011.01402.x
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2012
    detail.hit.zdb_id: 2041988-0
    detail.hit.zdb_id: 2050532-2
    SSG: 15,3
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  • 8
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    Online Resource
    Prenatal exposure to perfluorooctanesulfonate in rat resulted in long‐lasting changes of expression of synapsins and synaptophysin
    Wiley ; 2011
    In:  Synapse Vol. 65, No. 3 ( 2011-03), p. 225-233
    Details
    In: Synapse, Wiley, Vol. 65, No. 3 ( 2011-03), p. 225-233
    Abstract: Both animal and human studies have demonstrated that exposure to chemical pollutants during critical developmental period causes adverse consequences later in life. In uterus, perfluorooctanesulfonate (PFOS) exposure has been known to cause developmental neurotoxicity, such as increased motor activity, reduced habitation and impaired cognitive function. The possible mechanism of the impaired cognitive function induced by prenatal PFOS exposure was evaluated in this study. Pregnant Sprague Dawley (SD) rats were given 0.1, 0.6, and 2.0 mg kg −1 birth weight (bw) d −1 by gavage from gestation day (GD) 0 to GD20. Control received 0.5% Tween‐20 vehicle (4 ml kg −1 bw d −1 ). PFOS concentration in hippocampus of offspring was observed on postnatal day (PND) 0 and PND21. The ultrastructure of hippocampus and the gene expression of synaptic vesicle associated proteins in offspring hippocampus, which were important for the neurotransmitter release, were investigated. The transmission electron photomicrographs of the offspring hippocampus from PFOS‐treated maternal groups showed the ultrastructure of synapses was negatively affected. The offspring from PFOS‐treated maternal groups also differed significantly from controls with respect to the expression of synaptic vesicle associated proteins. The mRNA levels of synapsin1 (Syn1), synapsin2 (Syn2), and synaptophysin (Syp) were decreased in treated groups either on PND0 or on PND21. However, the mRNA level of synapsin3 (Syn3) decreased in 0.6‐ and 2.0‐mg kg −1 group on PND0, and showed no significant difference among control group and all treated groups on PND21. These results indicate that the impairment of cognitive function induced by PFOS may be attributed to the lower mRNA levels of synaptic vesicle associated proteins and the change of synaptic ultrastructure in hippocampus. Synapse, 2010. © 2010 Wiley‐Liss, Inc.
    Type of Medium: Online Resource
    ISSN: 0887-4476 , 1098-2396
    URL: Issue
    URL: Article
    DOI: 10.1002/syn.v65.3
    DOI: 10.1002/syn.20840
    Language: English
    Publisher: Wiley
    Publication Date: 2011
    detail.hit.zdb_id: 1474927-0
    SSG: 12
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  • 9
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    Daxx Mediates Oxidized Low-density Lipoprotein-Induced Cholesterol Accumulation and Apoptosis in Macrophages by Upregulating Caveolin-1 Expression* : Daxx Mediates Oxidized Low-density Lipoprotein-Induced Cholesterol Accumulation and Apoptosis in Macrophages by Upregulating Caveolin-1 Expression*
    China Science Publishing & Media Ltd. ; 2010
    In:  PROGRESS IN BIOCHEMISTRY AND BIOPHYSICS Vol. 37, No. 8 ( 2010-9-1), p. 881-890
    Details
    In: PROGRESS IN BIOCHEMISTRY AND BIOPHYSICS, China Science Publishing & Media Ltd., Vol. 37, No. 8 ( 2010-9-1), p. 881-890
    Type of Medium: Online Resource
    ISSN: 1000-3282
    URL: Article
    DOI: 10.3724/SP.J.1206.2010.00153
    Language: English
    Publisher: China Science Publishing & Media Ltd.
    Publication Date: 2010
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  • 10
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    Prenatal exposure to PFOS caused mitochondia‐mediated apoptosis in heart of weaned rat
    Wiley ; 2015
    In:  Environmental Toxicology Vol. 30, No. 9 ( 2015-09), p. 1082-1090
    Details
    In: Environmental Toxicology, Wiley, Vol. 30, No. 9 ( 2015-09), p. 1082-1090
    Abstract: Perfluorooctanyl sulfonate (PFOS), a cardiac toxicity compound, has been widely detected in the environment and in organisms. However, the toxic mechanism is not clear. Our previous study indicated that prenatal PFOS exposure led to swollen mitochondrial with vacuolar structure and loss of cristae in offsping's heart. The purpose of this study was to investigate the effect of PFOS on the apoptosis in developing heart and mitochondria‐mediated apoptosis pathway. Pregnant Sprague‐Dawley (SD) rats were exposed to PFOS at doses of 0.1, 0.6, and 2.0 mg/kg‐d and 0.05% Tween 80 as control by gavage from gestation day 2 (GD 2) to GD 21. Apoptosis, as well as expression of apoptosis related genes associated with mitochondrial‐mediated apoptosis pathway, including p53, bcl‐2, bax, cytochrome c, caspase‐9, and caspase‐3 were analyzed in heart tissues from weaned (postnatal day 21, PND 21) offspring. The results showed that prenatal PFOS exposure resulted in apoptosis in the offspring's heart. The mRNA and protein expression levels of p53, bax, cytochrome c, caspase‐9, and caspase‐3 in the offspring's heart were enhanced in various PFOS‐treated groups, meanwhile, the bcl‐2 expression levels were decreased. Our results indicated that prenatal PFOS exposure induced the apoptosis of weaned offspring rat heart tissue via mitochondria‐mediated apoptotic pathway. © 2014 Wiley Periodicals, Inc. Environ Toxicol 30: 1082–1090, 2015.
    Type of Medium: Online Resource
    ISSN: 1520-4081 , 1522-7278
    URL: Issue
    URL: Article
    DOI: 10.1002/tox.v30.9
    DOI: 10.1002/tox.21981
    Language: English
    Publisher: Wiley
    Publication Date: 2015
    detail.hit.zdb_id: 2027534-1
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