Plumbagin protects against hydrogen peroxide-induced neurotoxicity by modulating NF-κB and Nrf-2

Introduction : Redox signaling initiates pathogenesis of neuronal degeneration. Plumbagin is a potential antioxidant with anti-inflammatory, anti-cancer and radio sensitizing properties. In the present study, we aimed to determine the protective role of plumbagin against H 2 O 2 -induced neurotoxici...
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Gespeichert in:

Autor*in:	Wang Kuan-hong [verfasserIn] Li Bai-zhou [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2016

Schlagwörter:	H oxidative stress inflammation Nrf-2 neurotoxicity

Übergeordnetes Werk:	In: Archives of Medical Science - Termedia Publishing House, 2019, 14(2016), 5, Seite 1112-1118
Übergeordnetes Werk:	volume:14 ; year:2016 ; number:5 ; pages:1112-1118

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.5114/aoms.2016.64768

Katalog-ID:	DOAJ052414108

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520			\|a Introduction : Redox signaling initiates pathogenesis of neuronal degeneration. Plumbagin is a potential antioxidant with anti-inflammatory, anti-cancer and radio sensitizing properties. In the present study, we aimed to determine the protective role of plumbagin against H 2 O 2 -induced neurotoxicity in PC12 cells by determining nuclear factor κB (NF-κB) and nuclear factor E2-related factor 2 (Nrf-2) pathways. Material and methods : We analyzed oxidative stress by determining reactive oxygen species (ROS) and nitrite levels, and antioxidant enzyme activities. Nrf-2 and NF-κB p65 nuclear localization was determined through immunofluorescence. Further, nuclear levels of p-Nrf-2 and downstream expression of NAD(P)H quinone dehydrogenase 1 (NQO1), heme oxygenase-1 (HO-1) and glutathione-s-transferase (GST) were determined by western blot. Anti-inflammatory activity was analyzed by evaluating NF-B p65, cyclooxygenase-2 (COX-2) and interleukin (IL-6, IL-8, and MCP-1) expression. Results: The results showed that plumbagin increased (p < 0.01) the cell viability against H 2 O 2 -induced cell death in PC12 cells. Plumbagin effectively ameliorated H 2 O 2 -induced oxidative stress through reducing oxidative stress (p < 0.01) and activating p-Nrf-2 levels. Further, plumbagin up-regulated antioxidant enzyme activities (p < 0.01) against H 2 O 2 -induced oxidative stress. Plumbagin showed anti-inflammatory effect by suppressing NF-κB p65 activation and down-regulating NF-κB p65 and COX-2 expression. In addition, plumbagin modulated (p < 0.01) inflammatory cytokine expression against H 2 O 2 -induced neurotoxic effects. Conclusions : Together, our results show that plumbagin modulated NF-κB and Nrf-2 signaling. Thus, plumbagin might be an effective compound in preventing H 2 O 2 -induced neurotoxicity and its associated inflammatory responses.
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publishDate	2016
allfields	10.5114/aoms.2016.64768 doi (DE-627)DOAJ052414108 (DE-599)DOAJed60e40805ab443cbf4dbf5d4aa603fc DE-627 ger DE-627 rakwb eng Wang Kuan-hong verfasserin aut Plumbagin protects against hydrogen peroxide-induced neurotoxicity by modulating NF-κB and Nrf-2 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction : Redox signaling initiates pathogenesis of neuronal degeneration. Plumbagin is a potential antioxidant with anti-inflammatory, anti-cancer and radio sensitizing properties. In the present study, we aimed to determine the protective role of plumbagin against H 2 O 2 -induced neurotoxicity in PC12 cells by determining nuclear factor κB (NF-κB) and nuclear factor E2-related factor 2 (Nrf-2) pathways. Material and methods : We analyzed oxidative stress by determining reactive oxygen species (ROS) and nitrite levels, and antioxidant enzyme activities. Nrf-2 and NF-κB p65 nuclear localization was determined through immunofluorescence. Further, nuclear levels of p-Nrf-2 and downstream expression of NAD(P)H quinone dehydrogenase 1 (NQO1), heme oxygenase-1 (HO-1) and glutathione-s-transferase (GST) were determined by western blot. Anti-inflammatory activity was analyzed by evaluating NF-B p65, cyclooxygenase-2 (COX-2) and interleukin (IL-6, IL-8, and MCP-1) expression. Results: The results showed that plumbagin increased (p < 0.01) the cell viability against H 2 O 2 -induced cell death in PC12 cells. Plumbagin effectively ameliorated H 2 O 2 -induced oxidative stress through reducing oxidative stress (p < 0.01) and activating p-Nrf-2 levels. Further, plumbagin up-regulated antioxidant enzyme activities (p < 0.01) against H 2 O 2 -induced oxidative stress. Plumbagin showed anti-inflammatory effect by suppressing NF-κB p65 activation and down-regulating NF-κB p65 and COX-2 expression. In addition, plumbagin modulated (p < 0.01) inflammatory cytokine expression against H 2 O 2 -induced neurotoxic effects. Conclusions : Together, our results show that plumbagin modulated NF-κB and Nrf-2 signaling. Thus, plumbagin might be an effective compound in preventing H 2 O 2 -induced neurotoxicity and its associated inflammatory responses. H<SUB<2</SUB<O<SUB<2</SUB< oxidative stress inflammation Nrf-2 neurotoxicity Medicine R Li Bai-zhou verfasserin aut In Archives of Medical Science Termedia Publishing House, 2019 14(2016), 5, Seite 1112-1118 (DE-627)500321612 (DE-600)2203781-0 18969151 nnns volume:14 year:2016 number:5 pages:1112-1118 https://doi.org/10.5114/aoms.2016.64768 kostenfrei https://doaj.org/article/ed60e40805ab443cbf4dbf5d4aa603fc kostenfrei https://www.termedia.pl/Plumbagin-protects-against-hydrogen-peroxide-induced-neurotoxicity-by-modulating-NF-B-and-Nrf-2,19,28963,1,1.html kostenfrei https://doaj.org/toc/1734-1922 Journal toc kostenfrei https://doaj.org/toc/1896-9151 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 14 2016 5 1112-1118
spelling	10.5114/aoms.2016.64768 doi (DE-627)DOAJ052414108 (DE-599)DOAJed60e40805ab443cbf4dbf5d4aa603fc DE-627 ger DE-627 rakwb eng Wang Kuan-hong verfasserin aut Plumbagin protects against hydrogen peroxide-induced neurotoxicity by modulating NF-κB and Nrf-2 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction : Redox signaling initiates pathogenesis of neuronal degeneration. Plumbagin is a potential antioxidant with anti-inflammatory, anti-cancer and radio sensitizing properties. In the present study, we aimed to determine the protective role of plumbagin against H 2 O 2 -induced neurotoxicity in PC12 cells by determining nuclear factor κB (NF-κB) and nuclear factor E2-related factor 2 (Nrf-2) pathways. Material and methods : We analyzed oxidative stress by determining reactive oxygen species (ROS) and nitrite levels, and antioxidant enzyme activities. Nrf-2 and NF-κB p65 nuclear localization was determined through immunofluorescence. Further, nuclear levels of p-Nrf-2 and downstream expression of NAD(P)H quinone dehydrogenase 1 (NQO1), heme oxygenase-1 (HO-1) and glutathione-s-transferase (GST) were determined by western blot. Anti-inflammatory activity was analyzed by evaluating NF-B p65, cyclooxygenase-2 (COX-2) and interleukin (IL-6, IL-8, and MCP-1) expression. Results: The results showed that plumbagin increased (p < 0.01) the cell viability against H 2 O 2 -induced cell death in PC12 cells. Plumbagin effectively ameliorated H 2 O 2 -induced oxidative stress through reducing oxidative stress (p < 0.01) and activating p-Nrf-2 levels. Further, plumbagin up-regulated antioxidant enzyme activities (p < 0.01) against H 2 O 2 -induced oxidative stress. Plumbagin showed anti-inflammatory effect by suppressing NF-κB p65 activation and down-regulating NF-κB p65 and COX-2 expression. In addition, plumbagin modulated (p < 0.01) inflammatory cytokine expression against H 2 O 2 -induced neurotoxic effects. Conclusions : Together, our results show that plumbagin modulated NF-κB and Nrf-2 signaling. Thus, plumbagin might be an effective compound in preventing H 2 O 2 -induced neurotoxicity and its associated inflammatory responses. H<SUB<2</SUB<O<SUB<2</SUB< oxidative stress inflammation Nrf-2 neurotoxicity Medicine R Li Bai-zhou verfasserin aut In Archives of Medical Science Termedia Publishing House, 2019 14(2016), 5, Seite 1112-1118 (DE-627)500321612 (DE-600)2203781-0 18969151 nnns volume:14 year:2016 number:5 pages:1112-1118 https://doi.org/10.5114/aoms.2016.64768 kostenfrei https://doaj.org/article/ed60e40805ab443cbf4dbf5d4aa603fc kostenfrei https://www.termedia.pl/Plumbagin-protects-against-hydrogen-peroxide-induced-neurotoxicity-by-modulating-NF-B-and-Nrf-2,19,28963,1,1.html kostenfrei https://doaj.org/toc/1734-1922 Journal toc kostenfrei https://doaj.org/toc/1896-9151 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 14 2016 5 1112-1118
allfields_unstemmed	10.5114/aoms.2016.64768 doi (DE-627)DOAJ052414108 (DE-599)DOAJed60e40805ab443cbf4dbf5d4aa603fc DE-627 ger DE-627 rakwb eng Wang Kuan-hong verfasserin aut Plumbagin protects against hydrogen peroxide-induced neurotoxicity by modulating NF-κB and Nrf-2 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction : Redox signaling initiates pathogenesis of neuronal degeneration. Plumbagin is a potential antioxidant with anti-inflammatory, anti-cancer and radio sensitizing properties. In the present study, we aimed to determine the protective role of plumbagin against H 2 O 2 -induced neurotoxicity in PC12 cells by determining nuclear factor κB (NF-κB) and nuclear factor E2-related factor 2 (Nrf-2) pathways. Material and methods : We analyzed oxidative stress by determining reactive oxygen species (ROS) and nitrite levels, and antioxidant enzyme activities. Nrf-2 and NF-κB p65 nuclear localization was determined through immunofluorescence. Further, nuclear levels of p-Nrf-2 and downstream expression of NAD(P)H quinone dehydrogenase 1 (NQO1), heme oxygenase-1 (HO-1) and glutathione-s-transferase (GST) were determined by western blot. Anti-inflammatory activity was analyzed by evaluating NF-B p65, cyclooxygenase-2 (COX-2) and interleukin (IL-6, IL-8, and MCP-1) expression. Results: The results showed that plumbagin increased (p < 0.01) the cell viability against H 2 O 2 -induced cell death in PC12 cells. Plumbagin effectively ameliorated H 2 O 2 -induced oxidative stress through reducing oxidative stress (p < 0.01) and activating p-Nrf-2 levels. Further, plumbagin up-regulated antioxidant enzyme activities (p < 0.01) against H 2 O 2 -induced oxidative stress. Plumbagin showed anti-inflammatory effect by suppressing NF-κB p65 activation and down-regulating NF-κB p65 and COX-2 expression. In addition, plumbagin modulated (p < 0.01) inflammatory cytokine expression against H 2 O 2 -induced neurotoxic effects. Conclusions : Together, our results show that plumbagin modulated NF-κB and Nrf-2 signaling. Thus, plumbagin might be an effective compound in preventing H 2 O 2 -induced neurotoxicity and its associated inflammatory responses. H<SUB<2</SUB<O<SUB<2</SUB< oxidative stress inflammation Nrf-2 neurotoxicity Medicine R Li Bai-zhou verfasserin aut In Archives of Medical Science Termedia Publishing House, 2019 14(2016), 5, Seite 1112-1118 (DE-627)500321612 (DE-600)2203781-0 18969151 nnns volume:14 year:2016 number:5 pages:1112-1118 https://doi.org/10.5114/aoms.2016.64768 kostenfrei https://doaj.org/article/ed60e40805ab443cbf4dbf5d4aa603fc kostenfrei https://www.termedia.pl/Plumbagin-protects-against-hydrogen-peroxide-induced-neurotoxicity-by-modulating-NF-B-and-Nrf-2,19,28963,1,1.html kostenfrei https://doaj.org/toc/1734-1922 Journal toc kostenfrei https://doaj.org/toc/1896-9151 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 14 2016 5 1112-1118
allfieldsGer	10.5114/aoms.2016.64768 doi (DE-627)DOAJ052414108 (DE-599)DOAJed60e40805ab443cbf4dbf5d4aa603fc DE-627 ger DE-627 rakwb eng Wang Kuan-hong verfasserin aut Plumbagin protects against hydrogen peroxide-induced neurotoxicity by modulating NF-κB and Nrf-2 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction : Redox signaling initiates pathogenesis of neuronal degeneration. Plumbagin is a potential antioxidant with anti-inflammatory, anti-cancer and radio sensitizing properties. In the present study, we aimed to determine the protective role of plumbagin against H 2 O 2 -induced neurotoxicity in PC12 cells by determining nuclear factor κB (NF-κB) and nuclear factor E2-related factor 2 (Nrf-2) pathways. Material and methods : We analyzed oxidative stress by determining reactive oxygen species (ROS) and nitrite levels, and antioxidant enzyme activities. Nrf-2 and NF-κB p65 nuclear localization was determined through immunofluorescence. Further, nuclear levels of p-Nrf-2 and downstream expression of NAD(P)H quinone dehydrogenase 1 (NQO1), heme oxygenase-1 (HO-1) and glutathione-s-transferase (GST) were determined by western blot. Anti-inflammatory activity was analyzed by evaluating NF-B p65, cyclooxygenase-2 (COX-2) and interleukin (IL-6, IL-8, and MCP-1) expression. Results: The results showed that plumbagin increased (p < 0.01) the cell viability against H 2 O 2 -induced cell death in PC12 cells. Plumbagin effectively ameliorated H 2 O 2 -induced oxidative stress through reducing oxidative stress (p < 0.01) and activating p-Nrf-2 levels. Further, plumbagin up-regulated antioxidant enzyme activities (p < 0.01) against H 2 O 2 -induced oxidative stress. Plumbagin showed anti-inflammatory effect by suppressing NF-κB p65 activation and down-regulating NF-κB p65 and COX-2 expression. In addition, plumbagin modulated (p < 0.01) inflammatory cytokine expression against H 2 O 2 -induced neurotoxic effects. Conclusions : Together, our results show that plumbagin modulated NF-κB and Nrf-2 signaling. Thus, plumbagin might be an effective compound in preventing H 2 O 2 -induced neurotoxicity and its associated inflammatory responses. H<SUB<2</SUB<O<SUB<2</SUB< oxidative stress inflammation Nrf-2 neurotoxicity Medicine R Li Bai-zhou verfasserin aut In Archives of Medical Science Termedia Publishing House, 2019 14(2016), 5, Seite 1112-1118 (DE-627)500321612 (DE-600)2203781-0 18969151 nnns volume:14 year:2016 number:5 pages:1112-1118 https://doi.org/10.5114/aoms.2016.64768 kostenfrei https://doaj.org/article/ed60e40805ab443cbf4dbf5d4aa603fc kostenfrei https://www.termedia.pl/Plumbagin-protects-against-hydrogen-peroxide-induced-neurotoxicity-by-modulating-NF-B-and-Nrf-2,19,28963,1,1.html kostenfrei https://doaj.org/toc/1734-1922 Journal toc kostenfrei https://doaj.org/toc/1896-9151 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 14 2016 5 1112-1118
allfieldsSound	10.5114/aoms.2016.64768 doi (DE-627)DOAJ052414108 (DE-599)DOAJed60e40805ab443cbf4dbf5d4aa603fc DE-627 ger DE-627 rakwb eng Wang Kuan-hong verfasserin aut Plumbagin protects against hydrogen peroxide-induced neurotoxicity by modulating NF-κB and Nrf-2 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Introduction : Redox signaling initiates pathogenesis of neuronal degeneration. Plumbagin is a potential antioxidant with anti-inflammatory, anti-cancer and radio sensitizing properties. In the present study, we aimed to determine the protective role of plumbagin against H 2 O 2 -induced neurotoxicity in PC12 cells by determining nuclear factor κB (NF-κB) and nuclear factor E2-related factor 2 (Nrf-2) pathways. Material and methods : We analyzed oxidative stress by determining reactive oxygen species (ROS) and nitrite levels, and antioxidant enzyme activities. Nrf-2 and NF-κB p65 nuclear localization was determined through immunofluorescence. Further, nuclear levels of p-Nrf-2 and downstream expression of NAD(P)H quinone dehydrogenase 1 (NQO1), heme oxygenase-1 (HO-1) and glutathione-s-transferase (GST) were determined by western blot. Anti-inflammatory activity was analyzed by evaluating NF-B p65, cyclooxygenase-2 (COX-2) and interleukin (IL-6, IL-8, and MCP-1) expression. Results: The results showed that plumbagin increased (p < 0.01) the cell viability against H 2 O 2 -induced cell death in PC12 cells. Plumbagin effectively ameliorated H 2 O 2 -induced oxidative stress through reducing oxidative stress (p < 0.01) and activating p-Nrf-2 levels. Further, plumbagin up-regulated antioxidant enzyme activities (p < 0.01) against H 2 O 2 -induced oxidative stress. Plumbagin showed anti-inflammatory effect by suppressing NF-κB p65 activation and down-regulating NF-κB p65 and COX-2 expression. In addition, plumbagin modulated (p < 0.01) inflammatory cytokine expression against H 2 O 2 -induced neurotoxic effects. Conclusions : Together, our results show that plumbagin modulated NF-κB and Nrf-2 signaling. Thus, plumbagin might be an effective compound in preventing H 2 O 2 -induced neurotoxicity and its associated inflammatory responses. H<SUB<2</SUB<O<SUB<2</SUB< oxidative stress inflammation Nrf-2 neurotoxicity Medicine R Li Bai-zhou verfasserin aut In Archives of Medical Science Termedia Publishing House, 2019 14(2016), 5, Seite 1112-1118 (DE-627)500321612 (DE-600)2203781-0 18969151 nnns volume:14 year:2016 number:5 pages:1112-1118 https://doi.org/10.5114/aoms.2016.64768 kostenfrei https://doaj.org/article/ed60e40805ab443cbf4dbf5d4aa603fc kostenfrei https://www.termedia.pl/Plumbagin-protects-against-hydrogen-peroxide-induced-neurotoxicity-by-modulating-NF-B-and-Nrf-2,19,28963,1,1.html kostenfrei https://doaj.org/toc/1734-1922 Journal toc kostenfrei https://doaj.org/toc/1896-9151 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 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_2005 GBV_ILN_2009 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 14 2016 5 1112-1118
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Plumbagin is a potential antioxidant with anti-inflammatory, anti-cancer and radio sensitizing properties. In the present study, we aimed to determine the protective role of plumbagin against H 2 O 2 -induced neurotoxicity in PC12 cells by determining nuclear factor κB (NF-κB) and nuclear factor E2-related factor 2 (Nrf-2) pathways. Material and methods : We analyzed oxidative stress by determining reactive oxygen species (ROS) and nitrite levels, and antioxidant enzyme activities. Nrf-2 and NF-κB p65 nuclear localization was determined through immunofluorescence. Further, nuclear levels of p-Nrf-2 and downstream expression of NAD(P)H quinone dehydrogenase 1 (NQO1), heme oxygenase-1 (HO-1) and glutathione-s-transferase (GST) were determined by western blot. Anti-inflammatory activity was analyzed by evaluating NF-B p65, cyclooxygenase-2 (COX-2) and interleukin (IL-6, IL-8, and MCP-1) expression. 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title	Plumbagin protects against hydrogen peroxide-induced neurotoxicity by modulating NF-κB and Nrf-2
ctrlnum	(DE-627)DOAJ052414108 (DE-599)DOAJed60e40805ab443cbf4dbf5d4aa603fc
title_full	Plumbagin protects against hydrogen peroxide-induced neurotoxicity by modulating NF-κB and Nrf-2
author_sort	Wang Kuan-hong
journal	Archives of Medical Science
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author_browse	Wang Kuan-hong Li Bai-zhou
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format_se	Elektronische Aufsätze
author-letter	Wang Kuan-hong
doi_str_mv	10.5114/aoms.2016.64768
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title_sort	plumbagin protects against hydrogen peroxide-induced neurotoxicity by modulating nf-κb and nrf-2
title_auth	Plumbagin protects against hydrogen peroxide-induced neurotoxicity by modulating NF-κB and Nrf-2
abstract	Introduction : Redox signaling initiates pathogenesis of neuronal degeneration. Plumbagin is a potential antioxidant with anti-inflammatory, anti-cancer and radio sensitizing properties. In the present study, we aimed to determine the protective role of plumbagin against H 2 O 2 -induced neurotoxicity in PC12 cells by determining nuclear factor κB (NF-κB) and nuclear factor E2-related factor 2 (Nrf-2) pathways. Material and methods : We analyzed oxidative stress by determining reactive oxygen species (ROS) and nitrite levels, and antioxidant enzyme activities. Nrf-2 and NF-κB p65 nuclear localization was determined through immunofluorescence. Further, nuclear levels of p-Nrf-2 and downstream expression of NAD(P)H quinone dehydrogenase 1 (NQO1), heme oxygenase-1 (HO-1) and glutathione-s-transferase (GST) were determined by western blot. Anti-inflammatory activity was analyzed by evaluating NF-B p65, cyclooxygenase-2 (COX-2) and interleukin (IL-6, IL-8, and MCP-1) expression. Results: The results showed that plumbagin increased (p < 0.01) the cell viability against H 2 O 2 -induced cell death in PC12 cells. Plumbagin effectively ameliorated H 2 O 2 -induced oxidative stress through reducing oxidative stress (p < 0.01) and activating p-Nrf-2 levels. Further, plumbagin up-regulated antioxidant enzyme activities (p < 0.01) against H 2 O 2 -induced oxidative stress. Plumbagin showed anti-inflammatory effect by suppressing NF-κB p65 activation and down-regulating NF-κB p65 and COX-2 expression. In addition, plumbagin modulated (p < 0.01) inflammatory cytokine expression against H 2 O 2 -induced neurotoxic effects. Conclusions : Together, our results show that plumbagin modulated NF-κB and Nrf-2 signaling. Thus, plumbagin might be an effective compound in preventing H 2 O 2 -induced neurotoxicity and its associated inflammatory responses.
abstractGer	Introduction : Redox signaling initiates pathogenesis of neuronal degeneration. Plumbagin is a potential antioxidant with anti-inflammatory, anti-cancer and radio sensitizing properties. In the present study, we aimed to determine the protective role of plumbagin against H 2 O 2 -induced neurotoxicity in PC12 cells by determining nuclear factor κB (NF-κB) and nuclear factor E2-related factor 2 (Nrf-2) pathways. Material and methods : We analyzed oxidative stress by determining reactive oxygen species (ROS) and nitrite levels, and antioxidant enzyme activities. Nrf-2 and NF-κB p65 nuclear localization was determined through immunofluorescence. Further, nuclear levels of p-Nrf-2 and downstream expression of NAD(P)H quinone dehydrogenase 1 (NQO1), heme oxygenase-1 (HO-1) and glutathione-s-transferase (GST) were determined by western blot. Anti-inflammatory activity was analyzed by evaluating NF-B p65, cyclooxygenase-2 (COX-2) and interleukin (IL-6, IL-8, and MCP-1) expression. Results: The results showed that plumbagin increased (p < 0.01) the cell viability against H 2 O 2 -induced cell death in PC12 cells. Plumbagin effectively ameliorated H 2 O 2 -induced oxidative stress through reducing oxidative stress (p < 0.01) and activating p-Nrf-2 levels. Further, plumbagin up-regulated antioxidant enzyme activities (p < 0.01) against H 2 O 2 -induced oxidative stress. Plumbagin showed anti-inflammatory effect by suppressing NF-κB p65 activation and down-regulating NF-κB p65 and COX-2 expression. In addition, plumbagin modulated (p < 0.01) inflammatory cytokine expression against H 2 O 2 -induced neurotoxic effects. Conclusions : Together, our results show that plumbagin modulated NF-κB and Nrf-2 signaling. Thus, plumbagin might be an effective compound in preventing H 2 O 2 -induced neurotoxicity and its associated inflammatory responses.
abstract_unstemmed	Introduction : Redox signaling initiates pathogenesis of neuronal degeneration. Plumbagin is a potential antioxidant with anti-inflammatory, anti-cancer and radio sensitizing properties. In the present study, we aimed to determine the protective role of plumbagin against H 2 O 2 -induced neurotoxicity in PC12 cells by determining nuclear factor κB (NF-κB) and nuclear factor E2-related factor 2 (Nrf-2) pathways. Material and methods : We analyzed oxidative stress by determining reactive oxygen species (ROS) and nitrite levels, and antioxidant enzyme activities. Nrf-2 and NF-κB p65 nuclear localization was determined through immunofluorescence. Further, nuclear levels of p-Nrf-2 and downstream expression of NAD(P)H quinone dehydrogenase 1 (NQO1), heme oxygenase-1 (HO-1) and glutathione-s-transferase (GST) were determined by western blot. Anti-inflammatory activity was analyzed by evaluating NF-B p65, cyclooxygenase-2 (COX-2) and interleukin (IL-6, IL-8, and MCP-1) expression. Results: The results showed that plumbagin increased (p < 0.01) the cell viability against H 2 O 2 -induced cell death in PC12 cells. Plumbagin effectively ameliorated H 2 O 2 -induced oxidative stress through reducing oxidative stress (p < 0.01) and activating p-Nrf-2 levels. Further, plumbagin up-regulated antioxidant enzyme activities (p < 0.01) against H 2 O 2 -induced oxidative stress. Plumbagin showed anti-inflammatory effect by suppressing NF-κB p65 activation and down-regulating NF-κB p65 and COX-2 expression. In addition, plumbagin modulated (p < 0.01) inflammatory cytokine expression against H 2 O 2 -induced neurotoxic effects. Conclusions : Together, our results show that plumbagin modulated NF-κB and Nrf-2 signaling. Thus, plumbagin might be an effective compound in preventing H 2 O 2 -induced neurotoxicity and its associated inflammatory responses.
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container_issue	5
title_short	Plumbagin protects against hydrogen peroxide-induced neurotoxicity by modulating NF-κB and Nrf-2
url	https://doi.org/10.5114/aoms.2016.64768 https://doaj.org/article/ed60e40805ab443cbf4dbf5d4aa603fc https://www.termedia.pl/Plumbagin-protects-against-hydrogen-peroxide-induced-neurotoxicity-by-modulating-NF-B-and-Nrf-2,19,28963,1,1.html https://doaj.org/toc/1734-1922 https://doaj.org/toc/1896-9151
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up_date	2024-07-04T00:58:15.811Z
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