Neuroinflammation is induced by tongue-instilled ZnO nanoparticles via the $ Ca^{2+} $-dependent NF-κB and MAPK pathways
Background The extensive biological applications of zinc oxide nanoparticles (ZnO NPs) in stomatology have created serious concerns about their biotoxicity. In our previous study, ZnO NPs were confirmed to transfer to the central nervous system (CNS) via the taste nerve pathway and cause neurodegene...
Ausführliche Beschreibung
Autor*in: |
Liang, Huimin [verfasserIn] |
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E-Artikel |
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Englisch |
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2018 |
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Anmerkung: |
© The Author(s). 2018 |
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Übergeordnetes Werk: |
Enthalten in: Particle and fibre toxicology - London : BioMed Central, 2004, 15(2018), 1 vom: 19. Okt. |
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Übergeordnetes Werk: |
volume:15 ; year:2018 ; number:1 ; day:19 ; month:10 |
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DOI / URN: |
10.1186/s12989-018-0274-0 |
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SPR029301580 |
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520 | |a Background The extensive biological applications of zinc oxide nanoparticles (ZnO NPs) in stomatology have created serious concerns about their biotoxicity. In our previous study, ZnO NPs were confirmed to transfer to the central nervous system (CNS) via the taste nerve pathway and cause neurodegeneration after 30 days of tongue instillation. However, the potential adverse effects on the brain caused by tongue-instilled ZnO NPs are not fully known. Methods In this study, the biodistribution of Zn, cerebral histopathology and inflammatory responses were analysed after 30 days of ZnO NPs tongue instillation. Moreover, the molecular mechanisms underlying neuroinflammation in vivo were further elucidated by treating BV2 and PC12 cells with ZnO NPs in vitro. Results This analysis indicated that ZnO NPs can transfer into the CNS, activate glial cells and cause neuroinflammation after tongue instillation. Furthermore, exposure to ZnO NPs led to a reduction in cell viability and induction of inflammatory response and calcium influx in BV2 and PC12 cells. The mechanism underlying how ZnO NPs induce neuroinflammation via the $ Ca^{2+} $-dependent NF-κB, ERK and p38 activation pathways was verified at the cytological level. Conclusion This study provided a new way how NPs, such as ZnO NPs, induce neuroinflammation via the taste nerve translocation pathway, a new mechanism for ZnO NPs-induced neuroinflammation and a new direction for nanomaterial toxicity analysis. | ||
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700 | 1 | |a Lai, Xuan |4 aut | |
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700 | 1 | |a Wu, Junrong |4 aut | |
700 | 1 | |a Kang, Yiyuan |4 aut | |
700 | 1 | |a Wang, Xinying |4 aut | |
700 | 1 | |a Shao, Longquan |0 (orcid)0000-0002-3770-0815 |4 aut | |
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10.1186/s12989-018-0274-0 doi (DE-627)SPR029301580 (SPR)s12989-018-0274-0-e DE-627 ger DE-627 rakwb eng Liang, Huimin verfasserin aut Neuroinflammation is induced by tongue-instilled ZnO nanoparticles via the $ Ca^{2+} $-dependent NF-κB and MAPK pathways 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background The extensive biological applications of zinc oxide nanoparticles (ZnO NPs) in stomatology have created serious concerns about their biotoxicity. In our previous study, ZnO NPs were confirmed to transfer to the central nervous system (CNS) via the taste nerve pathway and cause neurodegeneration after 30 days of tongue instillation. However, the potential adverse effects on the brain caused by tongue-instilled ZnO NPs are not fully known. Methods In this study, the biodistribution of Zn, cerebral histopathology and inflammatory responses were analysed after 30 days of ZnO NPs tongue instillation. Moreover, the molecular mechanisms underlying neuroinflammation in vivo were further elucidated by treating BV2 and PC12 cells with ZnO NPs in vitro. Results This analysis indicated that ZnO NPs can transfer into the CNS, activate glial cells and cause neuroinflammation after tongue instillation. Furthermore, exposure to ZnO NPs led to a reduction in cell viability and induction of inflammatory response and calcium influx in BV2 and PC12 cells. The mechanism underlying how ZnO NPs induce neuroinflammation via the $ Ca^{2+} $-dependent NF-κB, ERK and p38 activation pathways was verified at the cytological level. Conclusion This study provided a new way how NPs, such as ZnO NPs, induce neuroinflammation via the taste nerve translocation pathway, a new mechanism for ZnO NPs-induced neuroinflammation and a new direction for nanomaterial toxicity analysis. Zinc oxide nanoparticles (dpeaa)DE-He213 Taste nerve (dpeaa)DE-He213 Neuroinflammation (dpeaa)DE-He213 Calcium ion (dpeaa)DE-He213 Chen, Aijie aut Lai, Xuan aut Liu, Jia aut Wu, Junrong aut Kang, Yiyuan aut Wang, Xinying aut Shao, Longquan (orcid)0000-0002-3770-0815 aut Enthalten in Particle and fibre toxicology London : BioMed Central, 2004 15(2018), 1 vom: 19. Okt. (DE-627)474928276 (DE-600)2170936-1 1743-8977 nnns volume:15 year:2018 number:1 day:19 month:10 https://dx.doi.org/10.1186/s12989-018-0274-0 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_2027 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2018 1 19 10 |
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10.1186/s12989-018-0274-0 doi (DE-627)SPR029301580 (SPR)s12989-018-0274-0-e DE-627 ger DE-627 rakwb eng Liang, Huimin verfasserin aut Neuroinflammation is induced by tongue-instilled ZnO nanoparticles via the $ Ca^{2+} $-dependent NF-κB and MAPK pathways 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background The extensive biological applications of zinc oxide nanoparticles (ZnO NPs) in stomatology have created serious concerns about their biotoxicity. In our previous study, ZnO NPs were confirmed to transfer to the central nervous system (CNS) via the taste nerve pathway and cause neurodegeneration after 30 days of tongue instillation. However, the potential adverse effects on the brain caused by tongue-instilled ZnO NPs are not fully known. Methods In this study, the biodistribution of Zn, cerebral histopathology and inflammatory responses were analysed after 30 days of ZnO NPs tongue instillation. Moreover, the molecular mechanisms underlying neuroinflammation in vivo were further elucidated by treating BV2 and PC12 cells with ZnO NPs in vitro. Results This analysis indicated that ZnO NPs can transfer into the CNS, activate glial cells and cause neuroinflammation after tongue instillation. Furthermore, exposure to ZnO NPs led to a reduction in cell viability and induction of inflammatory response and calcium influx in BV2 and PC12 cells. The mechanism underlying how ZnO NPs induce neuroinflammation via the $ Ca^{2+} $-dependent NF-κB, ERK and p38 activation pathways was verified at the cytological level. Conclusion This study provided a new way how NPs, such as ZnO NPs, induce neuroinflammation via the taste nerve translocation pathway, a new mechanism for ZnO NPs-induced neuroinflammation and a new direction for nanomaterial toxicity analysis. Zinc oxide nanoparticles (dpeaa)DE-He213 Taste nerve (dpeaa)DE-He213 Neuroinflammation (dpeaa)DE-He213 Calcium ion (dpeaa)DE-He213 Chen, Aijie aut Lai, Xuan aut Liu, Jia aut Wu, Junrong aut Kang, Yiyuan aut Wang, Xinying aut Shao, Longquan (orcid)0000-0002-3770-0815 aut Enthalten in Particle and fibre toxicology London : BioMed Central, 2004 15(2018), 1 vom: 19. Okt. (DE-627)474928276 (DE-600)2170936-1 1743-8977 nnns volume:15 year:2018 number:1 day:19 month:10 https://dx.doi.org/10.1186/s12989-018-0274-0 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_2027 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2018 1 19 10 |
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10.1186/s12989-018-0274-0 doi (DE-627)SPR029301580 (SPR)s12989-018-0274-0-e DE-627 ger DE-627 rakwb eng Liang, Huimin verfasserin aut Neuroinflammation is induced by tongue-instilled ZnO nanoparticles via the $ Ca^{2+} $-dependent NF-κB and MAPK pathways 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background The extensive biological applications of zinc oxide nanoparticles (ZnO NPs) in stomatology have created serious concerns about their biotoxicity. In our previous study, ZnO NPs were confirmed to transfer to the central nervous system (CNS) via the taste nerve pathway and cause neurodegeneration after 30 days of tongue instillation. However, the potential adverse effects on the brain caused by tongue-instilled ZnO NPs are not fully known. Methods In this study, the biodistribution of Zn, cerebral histopathology and inflammatory responses were analysed after 30 days of ZnO NPs tongue instillation. Moreover, the molecular mechanisms underlying neuroinflammation in vivo were further elucidated by treating BV2 and PC12 cells with ZnO NPs in vitro. Results This analysis indicated that ZnO NPs can transfer into the CNS, activate glial cells and cause neuroinflammation after tongue instillation. Furthermore, exposure to ZnO NPs led to a reduction in cell viability and induction of inflammatory response and calcium influx in BV2 and PC12 cells. The mechanism underlying how ZnO NPs induce neuroinflammation via the $ Ca^{2+} $-dependent NF-κB, ERK and p38 activation pathways was verified at the cytological level. Conclusion This study provided a new way how NPs, such as ZnO NPs, induce neuroinflammation via the taste nerve translocation pathway, a new mechanism for ZnO NPs-induced neuroinflammation and a new direction for nanomaterial toxicity analysis. Zinc oxide nanoparticles (dpeaa)DE-He213 Taste nerve (dpeaa)DE-He213 Neuroinflammation (dpeaa)DE-He213 Calcium ion (dpeaa)DE-He213 Chen, Aijie aut Lai, Xuan aut Liu, Jia aut Wu, Junrong aut Kang, Yiyuan aut Wang, Xinying aut Shao, Longquan (orcid)0000-0002-3770-0815 aut Enthalten in Particle and fibre toxicology London : BioMed Central, 2004 15(2018), 1 vom: 19. Okt. (DE-627)474928276 (DE-600)2170936-1 1743-8977 nnns volume:15 year:2018 number:1 day:19 month:10 https://dx.doi.org/10.1186/s12989-018-0274-0 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_2027 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2018 1 19 10 |
allfieldsGer |
10.1186/s12989-018-0274-0 doi (DE-627)SPR029301580 (SPR)s12989-018-0274-0-e DE-627 ger DE-627 rakwb eng Liang, Huimin verfasserin aut Neuroinflammation is induced by tongue-instilled ZnO nanoparticles via the $ Ca^{2+} $-dependent NF-κB and MAPK pathways 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background The extensive biological applications of zinc oxide nanoparticles (ZnO NPs) in stomatology have created serious concerns about their biotoxicity. In our previous study, ZnO NPs were confirmed to transfer to the central nervous system (CNS) via the taste nerve pathway and cause neurodegeneration after 30 days of tongue instillation. However, the potential adverse effects on the brain caused by tongue-instilled ZnO NPs are not fully known. Methods In this study, the biodistribution of Zn, cerebral histopathology and inflammatory responses were analysed after 30 days of ZnO NPs tongue instillation. Moreover, the molecular mechanisms underlying neuroinflammation in vivo were further elucidated by treating BV2 and PC12 cells with ZnO NPs in vitro. Results This analysis indicated that ZnO NPs can transfer into the CNS, activate glial cells and cause neuroinflammation after tongue instillation. Furthermore, exposure to ZnO NPs led to a reduction in cell viability and induction of inflammatory response and calcium influx in BV2 and PC12 cells. The mechanism underlying how ZnO NPs induce neuroinflammation via the $ Ca^{2+} $-dependent NF-κB, ERK and p38 activation pathways was verified at the cytological level. Conclusion This study provided a new way how NPs, such as ZnO NPs, induce neuroinflammation via the taste nerve translocation pathway, a new mechanism for ZnO NPs-induced neuroinflammation and a new direction for nanomaterial toxicity analysis. Zinc oxide nanoparticles (dpeaa)DE-He213 Taste nerve (dpeaa)DE-He213 Neuroinflammation (dpeaa)DE-He213 Calcium ion (dpeaa)DE-He213 Chen, Aijie aut Lai, Xuan aut Liu, Jia aut Wu, Junrong aut Kang, Yiyuan aut Wang, Xinying aut Shao, Longquan (orcid)0000-0002-3770-0815 aut Enthalten in Particle and fibre toxicology London : BioMed Central, 2004 15(2018), 1 vom: 19. Okt. (DE-627)474928276 (DE-600)2170936-1 1743-8977 nnns volume:15 year:2018 number:1 day:19 month:10 https://dx.doi.org/10.1186/s12989-018-0274-0 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_2027 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2018 1 19 10 |
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10.1186/s12989-018-0274-0 doi (DE-627)SPR029301580 (SPR)s12989-018-0274-0-e DE-627 ger DE-627 rakwb eng Liang, Huimin verfasserin aut Neuroinflammation is induced by tongue-instilled ZnO nanoparticles via the $ Ca^{2+} $-dependent NF-κB and MAPK pathways 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background The extensive biological applications of zinc oxide nanoparticles (ZnO NPs) in stomatology have created serious concerns about their biotoxicity. In our previous study, ZnO NPs were confirmed to transfer to the central nervous system (CNS) via the taste nerve pathway and cause neurodegeneration after 30 days of tongue instillation. However, the potential adverse effects on the brain caused by tongue-instilled ZnO NPs are not fully known. Methods In this study, the biodistribution of Zn, cerebral histopathology and inflammatory responses were analysed after 30 days of ZnO NPs tongue instillation. Moreover, the molecular mechanisms underlying neuroinflammation in vivo were further elucidated by treating BV2 and PC12 cells with ZnO NPs in vitro. Results This analysis indicated that ZnO NPs can transfer into the CNS, activate glial cells and cause neuroinflammation after tongue instillation. Furthermore, exposure to ZnO NPs led to a reduction in cell viability and induction of inflammatory response and calcium influx in BV2 and PC12 cells. The mechanism underlying how ZnO NPs induce neuroinflammation via the $ Ca^{2+} $-dependent NF-κB, ERK and p38 activation pathways was verified at the cytological level. Conclusion This study provided a new way how NPs, such as ZnO NPs, induce neuroinflammation via the taste nerve translocation pathway, a new mechanism for ZnO NPs-induced neuroinflammation and a new direction for nanomaterial toxicity analysis. Zinc oxide nanoparticles (dpeaa)DE-He213 Taste nerve (dpeaa)DE-He213 Neuroinflammation (dpeaa)DE-He213 Calcium ion (dpeaa)DE-He213 Chen, Aijie aut Lai, Xuan aut Liu, Jia aut Wu, Junrong aut Kang, Yiyuan aut Wang, Xinying aut Shao, Longquan (orcid)0000-0002-3770-0815 aut Enthalten in Particle and fibre toxicology London : BioMed Central, 2004 15(2018), 1 vom: 19. Okt. (DE-627)474928276 (DE-600)2170936-1 1743-8977 nnns volume:15 year:2018 number:1 day:19 month:10 https://dx.doi.org/10.1186/s12989-018-0274-0 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_2027 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 15 2018 1 19 10 |
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Liang, Huimin misc Zinc oxide nanoparticles misc Taste nerve misc Neuroinflammation misc Calcium ion Neuroinflammation is induced by tongue-instilled ZnO nanoparticles via the $ Ca^{2+} $-dependent NF-κB and MAPK pathways |
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Neuroinflammation is induced by tongue-instilled ZnO nanoparticles via the $ Ca^{2+} $-dependent NF-κB and MAPK pathways Zinc oxide nanoparticles (dpeaa)DE-He213 Taste nerve (dpeaa)DE-He213 Neuroinflammation (dpeaa)DE-He213 Calcium ion (dpeaa)DE-He213 |
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neuroinflammation is induced by tongue-instilled zno nanoparticles via the $ ca^{2+} $-dependent nf-κb and mapk pathways |
title_auth |
Neuroinflammation is induced by tongue-instilled ZnO nanoparticles via the $ Ca^{2+} $-dependent NF-κB and MAPK pathways |
abstract |
Background The extensive biological applications of zinc oxide nanoparticles (ZnO NPs) in stomatology have created serious concerns about their biotoxicity. In our previous study, ZnO NPs were confirmed to transfer to the central nervous system (CNS) via the taste nerve pathway and cause neurodegeneration after 30 days of tongue instillation. However, the potential adverse effects on the brain caused by tongue-instilled ZnO NPs are not fully known. Methods In this study, the biodistribution of Zn, cerebral histopathology and inflammatory responses were analysed after 30 days of ZnO NPs tongue instillation. Moreover, the molecular mechanisms underlying neuroinflammation in vivo were further elucidated by treating BV2 and PC12 cells with ZnO NPs in vitro. Results This analysis indicated that ZnO NPs can transfer into the CNS, activate glial cells and cause neuroinflammation after tongue instillation. Furthermore, exposure to ZnO NPs led to a reduction in cell viability and induction of inflammatory response and calcium influx in BV2 and PC12 cells. The mechanism underlying how ZnO NPs induce neuroinflammation via the $ Ca^{2+} $-dependent NF-κB, ERK and p38 activation pathways was verified at the cytological level. Conclusion This study provided a new way how NPs, such as ZnO NPs, induce neuroinflammation via the taste nerve translocation pathway, a new mechanism for ZnO NPs-induced neuroinflammation and a new direction for nanomaterial toxicity analysis. © The Author(s). 2018 |
abstractGer |
Background The extensive biological applications of zinc oxide nanoparticles (ZnO NPs) in stomatology have created serious concerns about their biotoxicity. In our previous study, ZnO NPs were confirmed to transfer to the central nervous system (CNS) via the taste nerve pathway and cause neurodegeneration after 30 days of tongue instillation. However, the potential adverse effects on the brain caused by tongue-instilled ZnO NPs are not fully known. Methods In this study, the biodistribution of Zn, cerebral histopathology and inflammatory responses were analysed after 30 days of ZnO NPs tongue instillation. Moreover, the molecular mechanisms underlying neuroinflammation in vivo were further elucidated by treating BV2 and PC12 cells with ZnO NPs in vitro. Results This analysis indicated that ZnO NPs can transfer into the CNS, activate glial cells and cause neuroinflammation after tongue instillation. Furthermore, exposure to ZnO NPs led to a reduction in cell viability and induction of inflammatory response and calcium influx in BV2 and PC12 cells. The mechanism underlying how ZnO NPs induce neuroinflammation via the $ Ca^{2+} $-dependent NF-κB, ERK and p38 activation pathways was verified at the cytological level. Conclusion This study provided a new way how NPs, such as ZnO NPs, induce neuroinflammation via the taste nerve translocation pathway, a new mechanism for ZnO NPs-induced neuroinflammation and a new direction for nanomaterial toxicity analysis. © The Author(s). 2018 |
abstract_unstemmed |
Background The extensive biological applications of zinc oxide nanoparticles (ZnO NPs) in stomatology have created serious concerns about their biotoxicity. In our previous study, ZnO NPs were confirmed to transfer to the central nervous system (CNS) via the taste nerve pathway and cause neurodegeneration after 30 days of tongue instillation. However, the potential adverse effects on the brain caused by tongue-instilled ZnO NPs are not fully known. Methods In this study, the biodistribution of Zn, cerebral histopathology and inflammatory responses were analysed after 30 days of ZnO NPs tongue instillation. Moreover, the molecular mechanisms underlying neuroinflammation in vivo were further elucidated by treating BV2 and PC12 cells with ZnO NPs in vitro. Results This analysis indicated that ZnO NPs can transfer into the CNS, activate glial cells and cause neuroinflammation after tongue instillation. Furthermore, exposure to ZnO NPs led to a reduction in cell viability and induction of inflammatory response and calcium influx in BV2 and PC12 cells. The mechanism underlying how ZnO NPs induce neuroinflammation via the $ Ca^{2+} $-dependent NF-κB, ERK and p38 activation pathways was verified at the cytological level. Conclusion This study provided a new way how NPs, such as ZnO NPs, induce neuroinflammation via the taste nerve translocation pathway, a new mechanism for ZnO NPs-induced neuroinflammation and a new direction for nanomaterial toxicity analysis. © The Author(s). 2018 |
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Neuroinflammation is induced by tongue-instilled ZnO nanoparticles via the $ Ca^{2+} $-dependent NF-κB and MAPK pathways |
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The mechanism underlying how ZnO NPs induce neuroinflammation via the $ Ca^{2+} $-dependent NF-κB, ERK and p38 activation pathways was verified at the cytological level. 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