Gastrodin Protects Neural Progenitor Cells Against Amyloid β (1–42)-Induced Neurotoxicity and Improves Hippocampal Neurogenesis in Amyloid β (1–42)-Injected Mice

Abstract The aim of this study was to investigate the neuroprotective effects of gastrodin (GAS), one of the major bioactive components of Gastrodia elata Blume (Tian Ma), against amyloid β (Aβ) (1–42)-induced neurotoxicity in primary neural progenitor cells (NPCs). We found that pretreatment with G...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Li, Meng [verfasserIn] Qian, Sumin [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2016

Schlagwörter:	Gastrodin Neural progenitor cells Amyloid β (1–42) Hippocampal neurogenesis

Übergeordnetes Werk:	Enthalten in: Journal of molecular neuroscience - New York, NY : Springer, 1998, 60(2016), 1 vom: 26. Apr., Seite 21-32
Übergeordnetes Werk:	volume:60 ; year:2016 ; number:1 ; day:26 ; month:04 ; pages:21-32

Links:	Volltext

DOI / URN:	10.1007/s12031-016-0758-z

Katalog-ID:	SPR023856467

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245	1	0	\|a Gastrodin Protects Neural Progenitor Cells Against Amyloid β (1–42)-Induced Neurotoxicity and Improves Hippocampal Neurogenesis in Amyloid β (1–42)-Injected Mice
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520			\|a Abstract The aim of this study was to investigate the neuroprotective effects of gastrodin (GAS), one of the major bioactive components of Gastrodia elata Blume (Tian Ma), against amyloid β (Aβ) (1–42)-induced neurotoxicity in primary neural progenitor cells (NPCs). We found that pretreatment with GAS not only prevents a loss in cell viability following treatment with Aβ (1–42) but also counteracts Aβ (1–42)-triggered release of pro-inflammatory cytokines and nitric oxide (NO) in a dose-dependent manner. Additionally, GAS was able to attenuate Aβ (1–42)-induced apoptosis in NPCs, evidenced by the decreased percentage of apoptotic cells and altered expression of apoptosis-related proteins in response to GAS pretreatment prior to Aβ (1–42) exposure. Furthermore, in Aβ (1–42)-injected C57BL/6 mice, we found that systemic administration of GAS could improve hippocampal neurogenesis, manifested by the increased number of SOX-2 and doublecortin (DCX)-positive cells in the DG area. Mechanistic studies revealed that in NPCs, GAS could reverse the Aβ (1–42)-induced increase in phosphorylation of MEK-1/2, extracellular signal-regulated kinases (ERK), and c-Jun N-terminal kinase (JNK). When combining GAS with the MEK inhibitor U0126 or the JNK inhibitor SP600125, we observed a synergistic effect against Aβ (1–42)-induced reduction in cell viability of NPCs. Taken together, these results show the efficacy and underlying mechanism of GAS against amyloid β (1–42)-induced neurotoxicity and provide substantial insight into the potential merits of GAS for its clinical application in the treatment of Alzheimer’s disease.
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912			\|a GBV_ILN_2055
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912			\|a GBV_ILN_2065
912			\|a GBV_ILN_2068
912			\|a GBV_ILN_2070
912			\|a GBV_ILN_2086
912			\|a GBV_ILN_2088
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912			\|a GBV_ILN_2106
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author_variant	m l ml s q sq
matchkey_str	article:15591166:2016----::atoipoetnuapoeioclsgisayod4idcdertxctadmrvsipcman
hierarchy_sort_str	2016
bklnumber	44.90
publishDate	2016
allfields	10.1007/s12031-016-0758-z doi (DE-627)SPR023856467 (SPR)s12031-016-0758-z-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Li, Meng verfasserin aut Gastrodin Protects Neural Progenitor Cells Against Amyloid β (1–42)-Induced Neurotoxicity and Improves Hippocampal Neurogenesis in Amyloid β (1–42)-Injected Mice 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The aim of this study was to investigate the neuroprotective effects of gastrodin (GAS), one of the major bioactive components of Gastrodia elata Blume (Tian Ma), against amyloid β (Aβ) (1–42)-induced neurotoxicity in primary neural progenitor cells (NPCs). We found that pretreatment with GAS not only prevents a loss in cell viability following treatment with Aβ (1–42) but also counteracts Aβ (1–42)-triggered release of pro-inflammatory cytokines and nitric oxide (NO) in a dose-dependent manner. Additionally, GAS was able to attenuate Aβ (1–42)-induced apoptosis in NPCs, evidenced by the decreased percentage of apoptotic cells and altered expression of apoptosis-related proteins in response to GAS pretreatment prior to Aβ (1–42) exposure. Furthermore, in Aβ (1–42)-injected C57BL/6 mice, we found that systemic administration of GAS could improve hippocampal neurogenesis, manifested by the increased number of SOX-2 and doublecortin (DCX)-positive cells in the DG area. Mechanistic studies revealed that in NPCs, GAS could reverse the Aβ (1–42)-induced increase in phosphorylation of MEK-1/2, extracellular signal-regulated kinases (ERK), and c-Jun N-terminal kinase (JNK). When combining GAS with the MEK inhibitor U0126 or the JNK inhibitor SP600125, we observed a synergistic effect against Aβ (1–42)-induced reduction in cell viability of NPCs. Taken together, these results show the efficacy and underlying mechanism of GAS against amyloid β (1–42)-induced neurotoxicity and provide substantial insight into the potential merits of GAS for its clinical application in the treatment of Alzheimer’s disease. Gastrodin (dpeaa)DE-He213 Neural progenitor cells (dpeaa)DE-He213 Amyloid β (1–42) (dpeaa)DE-He213 Hippocampal neurogenesis (dpeaa)DE-He213 Qian, Sumin verfasserin aut Enthalten in Journal of molecular neuroscience New York, NY : Springer, 1998 60(2016), 1 vom: 26. Apr., Seite 21-32 (DE-627)342319477 (DE-600)2071508-0 1559-1166 nnns volume:60 year:2016 number:1 day:26 month:04 pages:21-32 https://dx.doi.org/10.1007/s12031-016-0758-z lizenzpflichtig 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_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 60 2016 1 26 04 21-32
spelling	10.1007/s12031-016-0758-z doi (DE-627)SPR023856467 (SPR)s12031-016-0758-z-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Li, Meng verfasserin aut Gastrodin Protects Neural Progenitor Cells Against Amyloid β (1–42)-Induced Neurotoxicity and Improves Hippocampal Neurogenesis in Amyloid β (1–42)-Injected Mice 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The aim of this study was to investigate the neuroprotective effects of gastrodin (GAS), one of the major bioactive components of Gastrodia elata Blume (Tian Ma), against amyloid β (Aβ) (1–42)-induced neurotoxicity in primary neural progenitor cells (NPCs). We found that pretreatment with GAS not only prevents a loss in cell viability following treatment with Aβ (1–42) but also counteracts Aβ (1–42)-triggered release of pro-inflammatory cytokines and nitric oxide (NO) in a dose-dependent manner. Additionally, GAS was able to attenuate Aβ (1–42)-induced apoptosis in NPCs, evidenced by the decreased percentage of apoptotic cells and altered expression of apoptosis-related proteins in response to GAS pretreatment prior to Aβ (1–42) exposure. Furthermore, in Aβ (1–42)-injected C57BL/6 mice, we found that systemic administration of GAS could improve hippocampal neurogenesis, manifested by the increased number of SOX-2 and doublecortin (DCX)-positive cells in the DG area. Mechanistic studies revealed that in NPCs, GAS could reverse the Aβ (1–42)-induced increase in phosphorylation of MEK-1/2, extracellular signal-regulated kinases (ERK), and c-Jun N-terminal kinase (JNK). When combining GAS with the MEK inhibitor U0126 or the JNK inhibitor SP600125, we observed a synergistic effect against Aβ (1–42)-induced reduction in cell viability of NPCs. Taken together, these results show the efficacy and underlying mechanism of GAS against amyloid β (1–42)-induced neurotoxicity and provide substantial insight into the potential merits of GAS for its clinical application in the treatment of Alzheimer’s disease. Gastrodin (dpeaa)DE-He213 Neural progenitor cells (dpeaa)DE-He213 Amyloid β (1–42) (dpeaa)DE-He213 Hippocampal neurogenesis (dpeaa)DE-He213 Qian, Sumin verfasserin aut Enthalten in Journal of molecular neuroscience New York, NY : Springer, 1998 60(2016), 1 vom: 26. Apr., Seite 21-32 (DE-627)342319477 (DE-600)2071508-0 1559-1166 nnns volume:60 year:2016 number:1 day:26 month:04 pages:21-32 https://dx.doi.org/10.1007/s12031-016-0758-z lizenzpflichtig 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_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 60 2016 1 26 04 21-32
allfields_unstemmed	10.1007/s12031-016-0758-z doi (DE-627)SPR023856467 (SPR)s12031-016-0758-z-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Li, Meng verfasserin aut Gastrodin Protects Neural Progenitor Cells Against Amyloid β (1–42)-Induced Neurotoxicity and Improves Hippocampal Neurogenesis in Amyloid β (1–42)-Injected Mice 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The aim of this study was to investigate the neuroprotective effects of gastrodin (GAS), one of the major bioactive components of Gastrodia elata Blume (Tian Ma), against amyloid β (Aβ) (1–42)-induced neurotoxicity in primary neural progenitor cells (NPCs). We found that pretreatment with GAS not only prevents a loss in cell viability following treatment with Aβ (1–42) but also counteracts Aβ (1–42)-triggered release of pro-inflammatory cytokines and nitric oxide (NO) in a dose-dependent manner. Additionally, GAS was able to attenuate Aβ (1–42)-induced apoptosis in NPCs, evidenced by the decreased percentage of apoptotic cells and altered expression of apoptosis-related proteins in response to GAS pretreatment prior to Aβ (1–42) exposure. Furthermore, in Aβ (1–42)-injected C57BL/6 mice, we found that systemic administration of GAS could improve hippocampal neurogenesis, manifested by the increased number of SOX-2 and doublecortin (DCX)-positive cells in the DG area. Mechanistic studies revealed that in NPCs, GAS could reverse the Aβ (1–42)-induced increase in phosphorylation of MEK-1/2, extracellular signal-regulated kinases (ERK), and c-Jun N-terminal kinase (JNK). When combining GAS with the MEK inhibitor U0126 or the JNK inhibitor SP600125, we observed a synergistic effect against Aβ (1–42)-induced reduction in cell viability of NPCs. Taken together, these results show the efficacy and underlying mechanism of GAS against amyloid β (1–42)-induced neurotoxicity and provide substantial insight into the potential merits of GAS for its clinical application in the treatment of Alzheimer’s disease. Gastrodin (dpeaa)DE-He213 Neural progenitor cells (dpeaa)DE-He213 Amyloid β (1–42) (dpeaa)DE-He213 Hippocampal neurogenesis (dpeaa)DE-He213 Qian, Sumin verfasserin aut Enthalten in Journal of molecular neuroscience New York, NY : Springer, 1998 60(2016), 1 vom: 26. Apr., Seite 21-32 (DE-627)342319477 (DE-600)2071508-0 1559-1166 nnns volume:60 year:2016 number:1 day:26 month:04 pages:21-32 https://dx.doi.org/10.1007/s12031-016-0758-z lizenzpflichtig 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_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 60 2016 1 26 04 21-32
allfieldsGer	10.1007/s12031-016-0758-z doi (DE-627)SPR023856467 (SPR)s12031-016-0758-z-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Li, Meng verfasserin aut Gastrodin Protects Neural Progenitor Cells Against Amyloid β (1–42)-Induced Neurotoxicity and Improves Hippocampal Neurogenesis in Amyloid β (1–42)-Injected Mice 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The aim of this study was to investigate the neuroprotective effects of gastrodin (GAS), one of the major bioactive components of Gastrodia elata Blume (Tian Ma), against amyloid β (Aβ) (1–42)-induced neurotoxicity in primary neural progenitor cells (NPCs). We found that pretreatment with GAS not only prevents a loss in cell viability following treatment with Aβ (1–42) but also counteracts Aβ (1–42)-triggered release of pro-inflammatory cytokines and nitric oxide (NO) in a dose-dependent manner. Additionally, GAS was able to attenuate Aβ (1–42)-induced apoptosis in NPCs, evidenced by the decreased percentage of apoptotic cells and altered expression of apoptosis-related proteins in response to GAS pretreatment prior to Aβ (1–42) exposure. Furthermore, in Aβ (1–42)-injected C57BL/6 mice, we found that systemic administration of GAS could improve hippocampal neurogenesis, manifested by the increased number of SOX-2 and doublecortin (DCX)-positive cells in the DG area. Mechanistic studies revealed that in NPCs, GAS could reverse the Aβ (1–42)-induced increase in phosphorylation of MEK-1/2, extracellular signal-regulated kinases (ERK), and c-Jun N-terminal kinase (JNK). When combining GAS with the MEK inhibitor U0126 or the JNK inhibitor SP600125, we observed a synergistic effect against Aβ (1–42)-induced reduction in cell viability of NPCs. Taken together, these results show the efficacy and underlying mechanism of GAS against amyloid β (1–42)-induced neurotoxicity and provide substantial insight into the potential merits of GAS for its clinical application in the treatment of Alzheimer’s disease. Gastrodin (dpeaa)DE-He213 Neural progenitor cells (dpeaa)DE-He213 Amyloid β (1–42) (dpeaa)DE-He213 Hippocampal neurogenesis (dpeaa)DE-He213 Qian, Sumin verfasserin aut Enthalten in Journal of molecular neuroscience New York, NY : Springer, 1998 60(2016), 1 vom: 26. Apr., Seite 21-32 (DE-627)342319477 (DE-600)2071508-0 1559-1166 nnns volume:60 year:2016 number:1 day:26 month:04 pages:21-32 https://dx.doi.org/10.1007/s12031-016-0758-z lizenzpflichtig 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_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 60 2016 1 26 04 21-32
allfieldsSound	10.1007/s12031-016-0758-z doi (DE-627)SPR023856467 (SPR)s12031-016-0758-z-e DE-627 ger DE-627 rakwb eng 610 ASE 44.90 bkl Li, Meng verfasserin aut Gastrodin Protects Neural Progenitor Cells Against Amyloid β (1–42)-Induced Neurotoxicity and Improves Hippocampal Neurogenesis in Amyloid β (1–42)-Injected Mice 2016 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The aim of this study was to investigate the neuroprotective effects of gastrodin (GAS), one of the major bioactive components of Gastrodia elata Blume (Tian Ma), against amyloid β (Aβ) (1–42)-induced neurotoxicity in primary neural progenitor cells (NPCs). We found that pretreatment with GAS not only prevents a loss in cell viability following treatment with Aβ (1–42) but also counteracts Aβ (1–42)-triggered release of pro-inflammatory cytokines and nitric oxide (NO) in a dose-dependent manner. Additionally, GAS was able to attenuate Aβ (1–42)-induced apoptosis in NPCs, evidenced by the decreased percentage of apoptotic cells and altered expression of apoptosis-related proteins in response to GAS pretreatment prior to Aβ (1–42) exposure. Furthermore, in Aβ (1–42)-injected C57BL/6 mice, we found that systemic administration of GAS could improve hippocampal neurogenesis, manifested by the increased number of SOX-2 and doublecortin (DCX)-positive cells in the DG area. Mechanistic studies revealed that in NPCs, GAS could reverse the Aβ (1–42)-induced increase in phosphorylation of MEK-1/2, extracellular signal-regulated kinases (ERK), and c-Jun N-terminal kinase (JNK). When combining GAS with the MEK inhibitor U0126 or the JNK inhibitor SP600125, we observed a synergistic effect against Aβ (1–42)-induced reduction in cell viability of NPCs. Taken together, these results show the efficacy and underlying mechanism of GAS against amyloid β (1–42)-induced neurotoxicity and provide substantial insight into the potential merits of GAS for its clinical application in the treatment of Alzheimer’s disease. Gastrodin (dpeaa)DE-He213 Neural progenitor cells (dpeaa)DE-He213 Amyloid β (1–42) (dpeaa)DE-He213 Hippocampal neurogenesis (dpeaa)DE-He213 Qian, Sumin verfasserin aut Enthalten in Journal of molecular neuroscience New York, NY : Springer, 1998 60(2016), 1 vom: 26. Apr., Seite 21-32 (DE-627)342319477 (DE-600)2071508-0 1559-1166 nnns volume:60 year:2016 number:1 day:26 month:04 pages:21-32 https://dx.doi.org/10.1007/s12031-016-0758-z lizenzpflichtig 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_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 ASE AR 60 2016 1 26 04 21-32
language	English
source	Enthalten in Journal of molecular neuroscience 60(2016), 1 vom: 26. Apr., Seite 21-32 volume:60 year:2016 number:1 day:26 month:04 pages:21-32
sourceStr	Enthalten in Journal of molecular neuroscience 60(2016), 1 vom: 26. Apr., Seite 21-32 volume:60 year:2016 number:1 day:26 month:04 pages:21-32
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Gastrodin Neural progenitor cells Amyloid β (1–42) Hippocampal neurogenesis
dewey-raw	610
isfreeaccess_bool	false
container_title	Journal of molecular neuroscience
authorswithroles_txt_mv	Li, Meng @@aut@@ Qian, Sumin @@aut@@
publishDateDaySort_date	2016-04-26T00:00:00Z
hierarchy_top_id	342319477
dewey-sort	3610
id	SPR023856467
language_de	englisch
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author	Li, Meng
spellingShingle	Li, Meng ddc 610 bkl 44.90 misc Gastrodin misc Neural progenitor cells misc Amyloid β (1–42) misc Hippocampal neurogenesis Gastrodin Protects Neural Progenitor Cells Against Amyloid β (1–42)-Induced Neurotoxicity and Improves Hippocampal Neurogenesis in Amyloid β (1–42)-Injected Mice
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topic_title	610 ASE 44.90 bkl Gastrodin Protects Neural Progenitor Cells Against Amyloid β (1–42)-Induced Neurotoxicity and Improves Hippocampal Neurogenesis in Amyloid β (1–42)-Injected Mice Gastrodin (dpeaa)DE-He213 Neural progenitor cells (dpeaa)DE-He213 Amyloid β (1–42) (dpeaa)DE-He213 Hippocampal neurogenesis (dpeaa)DE-He213
topic	ddc 610 bkl 44.90 misc Gastrodin misc Neural progenitor cells misc Amyloid β (1–42) misc Hippocampal neurogenesis
topic_unstemmed	ddc 610 bkl 44.90 misc Gastrodin misc Neural progenitor cells misc Amyloid β (1–42) misc Hippocampal neurogenesis
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title	Gastrodin Protects Neural Progenitor Cells Against Amyloid β (1–42)-Induced Neurotoxicity and Improves Hippocampal Neurogenesis in Amyloid β (1–42)-Injected Mice
ctrlnum	(DE-627)SPR023856467 (SPR)s12031-016-0758-z-e
title_full	Gastrodin Protects Neural Progenitor Cells Against Amyloid β (1–42)-Induced Neurotoxicity and Improves Hippocampal Neurogenesis in Amyloid β (1–42)-Injected Mice
author_sort	Li, Meng
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title_sort	gastrodin protects neural progenitor cells against amyloid β (1–42)-induced neurotoxicity and improves hippocampal neurogenesis in amyloid β (1–42)-injected mice
title_auth	Gastrodin Protects Neural Progenitor Cells Against Amyloid β (1–42)-Induced Neurotoxicity and Improves Hippocampal Neurogenesis in Amyloid β (1–42)-Injected Mice
abstract	Abstract The aim of this study was to investigate the neuroprotective effects of gastrodin (GAS), one of the major bioactive components of Gastrodia elata Blume (Tian Ma), against amyloid β (Aβ) (1–42)-induced neurotoxicity in primary neural progenitor cells (NPCs). We found that pretreatment with GAS not only prevents a loss in cell viability following treatment with Aβ (1–42) but also counteracts Aβ (1–42)-triggered release of pro-inflammatory cytokines and nitric oxide (NO) in a dose-dependent manner. Additionally, GAS was able to attenuate Aβ (1–42)-induced apoptosis in NPCs, evidenced by the decreased percentage of apoptotic cells and altered expression of apoptosis-related proteins in response to GAS pretreatment prior to Aβ (1–42) exposure. Furthermore, in Aβ (1–42)-injected C57BL/6 mice, we found that systemic administration of GAS could improve hippocampal neurogenesis, manifested by the increased number of SOX-2 and doublecortin (DCX)-positive cells in the DG area. Mechanistic studies revealed that in NPCs, GAS could reverse the Aβ (1–42)-induced increase in phosphorylation of MEK-1/2, extracellular signal-regulated kinases (ERK), and c-Jun N-terminal kinase (JNK). When combining GAS with the MEK inhibitor U0126 or the JNK inhibitor SP600125, we observed a synergistic effect against Aβ (1–42)-induced reduction in cell viability of NPCs. Taken together, these results show the efficacy and underlying mechanism of GAS against amyloid β (1–42)-induced neurotoxicity and provide substantial insight into the potential merits of GAS for its clinical application in the treatment of Alzheimer’s disease.
abstractGer	Abstract The aim of this study was to investigate the neuroprotective effects of gastrodin (GAS), one of the major bioactive components of Gastrodia elata Blume (Tian Ma), against amyloid β (Aβ) (1–42)-induced neurotoxicity in primary neural progenitor cells (NPCs). We found that pretreatment with GAS not only prevents a loss in cell viability following treatment with Aβ (1–42) but also counteracts Aβ (1–42)-triggered release of pro-inflammatory cytokines and nitric oxide (NO) in a dose-dependent manner. Additionally, GAS was able to attenuate Aβ (1–42)-induced apoptosis in NPCs, evidenced by the decreased percentage of apoptotic cells and altered expression of apoptosis-related proteins in response to GAS pretreatment prior to Aβ (1–42) exposure. Furthermore, in Aβ (1–42)-injected C57BL/6 mice, we found that systemic administration of GAS could improve hippocampal neurogenesis, manifested by the increased number of SOX-2 and doublecortin (DCX)-positive cells in the DG area. Mechanistic studies revealed that in NPCs, GAS could reverse the Aβ (1–42)-induced increase in phosphorylation of MEK-1/2, extracellular signal-regulated kinases (ERK), and c-Jun N-terminal kinase (JNK). When combining GAS with the MEK inhibitor U0126 or the JNK inhibitor SP600125, we observed a synergistic effect against Aβ (1–42)-induced reduction in cell viability of NPCs. Taken together, these results show the efficacy and underlying mechanism of GAS against amyloid β (1–42)-induced neurotoxicity and provide substantial insight into the potential merits of GAS for its clinical application in the treatment of Alzheimer’s disease.
abstract_unstemmed	Abstract The aim of this study was to investigate the neuroprotective effects of gastrodin (GAS), one of the major bioactive components of Gastrodia elata Blume (Tian Ma), against amyloid β (Aβ) (1–42)-induced neurotoxicity in primary neural progenitor cells (NPCs). We found that pretreatment with GAS not only prevents a loss in cell viability following treatment with Aβ (1–42) but also counteracts Aβ (1–42)-triggered release of pro-inflammatory cytokines and nitric oxide (NO) in a dose-dependent manner. Additionally, GAS was able to attenuate Aβ (1–42)-induced apoptosis in NPCs, evidenced by the decreased percentage of apoptotic cells and altered expression of apoptosis-related proteins in response to GAS pretreatment prior to Aβ (1–42) exposure. Furthermore, in Aβ (1–42)-injected C57BL/6 mice, we found that systemic administration of GAS could improve hippocampal neurogenesis, manifested by the increased number of SOX-2 and doublecortin (DCX)-positive cells in the DG area. Mechanistic studies revealed that in NPCs, GAS could reverse the Aβ (1–42)-induced increase in phosphorylation of MEK-1/2, extracellular signal-regulated kinases (ERK), and c-Jun N-terminal kinase (JNK). When combining GAS with the MEK inhibitor U0126 or the JNK inhibitor SP600125, we observed a synergistic effect against Aβ (1–42)-induced reduction in cell viability of NPCs. Taken together, these results show the efficacy and underlying mechanism of GAS against amyloid β (1–42)-induced neurotoxicity and provide substantial insight into the potential merits of GAS for its clinical application in the treatment of Alzheimer’s disease.
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container_issue	1
title_short	Gastrodin Protects Neural Progenitor Cells Against Amyloid β (1–42)-Induced Neurotoxicity and Improves Hippocampal Neurogenesis in Amyloid β (1–42)-Injected Mice
url	https://dx.doi.org/10.1007/s12031-016-0758-z
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author2	Qian, Sumin
author2Str	Qian, Sumin
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doi_str	10.1007/s12031-016-0758-z
up_date	2024-07-03T21:51:40.834Z
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Gastrodin Protects Neural Progenitor Cells Against Amyloid β (1–42)-Induced Neurotoxicity and Improves Hippocampal Neurogenesis in Amyloid β (1–42)-Injected Mice

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