In vitro ischemic preconditioning mediates the Ca 2+ /CaN/NFAT pathway to protect against oxygen-glucose deprivation-induced cellular damage and inflammatory responses

Oxygen-glucose deprivation (OGD) is a critical model for studying hypoxic-ischemic cerebrovascular disease in vitro. This paper is to investigate the protection of OGD-induced cellular damage and inflammatory responses by OGD preconditioning in vitro, to provide a theoretical basis for OGD precondit...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Zhang, Lihong [verfasserIn] Guo, Qingzi [verfasserIn] An, Ran [verfasserIn] Shen, Shuhan [verfasserIn] Yin, Lin [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	Oxygen-glucose deprivation Oxygen-glucose deprivation preconditioning Ca2+/CaN/NFAT pathway Cell viability Apoptosis Inflammatory factors

Übergeordnetes Werk:	Enthalten in: Brain research - Amsterdam : Elsevier, 1966, 1826
Übergeordnetes Werk:	volume:1826

DOI / URN:	10.1016/j.brainres.2023.148736

Katalog-ID:	ELV066998611

Internformat


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245	1	0	\|a In vitro ischemic preconditioning mediates the Ca 2+ /CaN/NFAT pathway to protect against oxygen-glucose deprivation-induced cellular damage and inflammatory responses
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520			\|a Oxygen-glucose deprivation (OGD) is a critical model for studying hypoxic-ischemic cerebrovascular disease in vitro. This paper is to investigate the protection of OGD-induced cellular damage and inflammatory responses by OGD preconditioning in vitro, to provide a theoretical basis for OGD preconditioning to improve the prevention and prognosis of ischemic stroke. OGD or OGD preconditioning model was established by culturing the PC12 cell line in vitro, followed by further adding A23187 (calcium ion carrier) or CsA (calcium ion antagonist). Cell viability was detected by MTT, apoptosis by Hoechst 33,258 staining, the levels of TNF-α and IL-1β mRNA by RT-qPCR and ELISA, and the levels of CaN, NFAT, COX-2 by RT-qPCR and Western blot. Cell viability was decreased, and apoptosis, inflammatory cytokines, and CaN, NFAT, and COX-2 levels were notably increased upon OGD, while OGD pretreatment significantly increased cell viability and decreased apoptosis, inflammation, and the Ca2+/CaN/NFAT pathway. Treatment with A23187 decreased cell viability, promoted apoptosis, and significantly increased TNF-α, IL-1β, CaN, NFAT, and COX-2 levels, while CsA treatment reduced the opposite results. In vitro OGD preconditioning mediates the Ca2+/CaN/NFAT pathway to protect against OGD-induced cellular damage and inflammatory responses.
650		4	\|a Oxygen-glucose deprivation
650		4	\|a Oxygen-glucose deprivation preconditioning
650		4	\|a Ca2+/CaN/NFAT pathway
650		4	\|a Cell viability
650		4	\|a Apoptosis
650		4	\|a Inflammatory factors
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700	1		\|a An, Ran \|e verfasserin \|4 aut
700	1		\|a Shen, Shuhan \|e verfasserin \|4 aut
700	1		\|a Yin, Lin \|e verfasserin \|0 (orcid)0009-0008-8711-4188 \|4 aut
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936	b	k	\|a 44.90 \|j Neurologie \|q VZ
951			\|a AR
952			\|d 1826

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publishDate	2023
allfields	10.1016/j.brainres.2023.148736 doi (DE-627)ELV066998611 (ELSEVIER)S0006-8993(23)00507-3 DE-627 ger DE-627 rda eng 150 610 VZ 44.90 bkl Zhang, Lihong verfasserin aut In vitro ischemic preconditioning mediates the Ca 2+ /CaN/NFAT pathway to protect against oxygen-glucose deprivation-induced cellular damage and inflammatory responses 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Oxygen-glucose deprivation (OGD) is a critical model for studying hypoxic-ischemic cerebrovascular disease in vitro. This paper is to investigate the protection of OGD-induced cellular damage and inflammatory responses by OGD preconditioning in vitro, to provide a theoretical basis for OGD preconditioning to improve the prevention and prognosis of ischemic stroke. OGD or OGD preconditioning model was established by culturing the PC12 cell line in vitro, followed by further adding A23187 (calcium ion carrier) or CsA (calcium ion antagonist). Cell viability was detected by MTT, apoptosis by Hoechst 33,258 staining, the levels of TNF-α and IL-1β mRNA by RT-qPCR and ELISA, and the levels of CaN, NFAT, COX-2 by RT-qPCR and Western blot. Cell viability was decreased, and apoptosis, inflammatory cytokines, and CaN, NFAT, and COX-2 levels were notably increased upon OGD, while OGD pretreatment significantly increased cell viability and decreased apoptosis, inflammation, and the Ca2+/CaN/NFAT pathway. Treatment with A23187 decreased cell viability, promoted apoptosis, and significantly increased TNF-α, IL-1β, CaN, NFAT, and COX-2 levels, while CsA treatment reduced the opposite results. In vitro OGD preconditioning mediates the Ca2+/CaN/NFAT pathway to protect against OGD-induced cellular damage and inflammatory responses. Oxygen-glucose deprivation Oxygen-glucose deprivation preconditioning Ca2+/CaN/NFAT pathway Cell viability Apoptosis Inflammatory factors Guo, Qingzi verfasserin aut An, Ran verfasserin aut Shen, Shuhan verfasserin aut Yin, Lin verfasserin (orcid)0009-0008-8711-4188 aut Enthalten in Brain research Amsterdam : Elsevier, 1966 1826 Online-Ressource (DE-627)254635776 (DE-600)1462674-3 (DE-576)074530976 1872-6240 nnns volume:1826 GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 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_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 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_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 Neurologie VZ AR 1826
spelling	10.1016/j.brainres.2023.148736 doi (DE-627)ELV066998611 (ELSEVIER)S0006-8993(23)00507-3 DE-627 ger DE-627 rda eng 150 610 VZ 44.90 bkl Zhang, Lihong verfasserin aut In vitro ischemic preconditioning mediates the Ca 2+ /CaN/NFAT pathway to protect against oxygen-glucose deprivation-induced cellular damage and inflammatory responses 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Oxygen-glucose deprivation (OGD) is a critical model for studying hypoxic-ischemic cerebrovascular disease in vitro. This paper is to investigate the protection of OGD-induced cellular damage and inflammatory responses by OGD preconditioning in vitro, to provide a theoretical basis for OGD preconditioning to improve the prevention and prognosis of ischemic stroke. OGD or OGD preconditioning model was established by culturing the PC12 cell line in vitro, followed by further adding A23187 (calcium ion carrier) or CsA (calcium ion antagonist). Cell viability was detected by MTT, apoptosis by Hoechst 33,258 staining, the levels of TNF-α and IL-1β mRNA by RT-qPCR and ELISA, and the levels of CaN, NFAT, COX-2 by RT-qPCR and Western blot. Cell viability was decreased, and apoptosis, inflammatory cytokines, and CaN, NFAT, and COX-2 levels were notably increased upon OGD, while OGD pretreatment significantly increased cell viability and decreased apoptosis, inflammation, and the Ca2+/CaN/NFAT pathway. Treatment with A23187 decreased cell viability, promoted apoptosis, and significantly increased TNF-α, IL-1β, CaN, NFAT, and COX-2 levels, while CsA treatment reduced the opposite results. In vitro OGD preconditioning mediates the Ca2+/CaN/NFAT pathway to protect against OGD-induced cellular damage and inflammatory responses. Oxygen-glucose deprivation Oxygen-glucose deprivation preconditioning Ca2+/CaN/NFAT pathway Cell viability Apoptosis Inflammatory factors Guo, Qingzi verfasserin aut An, Ran verfasserin aut Shen, Shuhan verfasserin aut Yin, Lin verfasserin (orcid)0009-0008-8711-4188 aut Enthalten in Brain research Amsterdam : Elsevier, 1966 1826 Online-Ressource (DE-627)254635776 (DE-600)1462674-3 (DE-576)074530976 1872-6240 nnns volume:1826 GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 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_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 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_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 Neurologie VZ AR 1826
allfields_unstemmed	10.1016/j.brainres.2023.148736 doi (DE-627)ELV066998611 (ELSEVIER)S0006-8993(23)00507-3 DE-627 ger DE-627 rda eng 150 610 VZ 44.90 bkl Zhang, Lihong verfasserin aut In vitro ischemic preconditioning mediates the Ca 2+ /CaN/NFAT pathway to protect against oxygen-glucose deprivation-induced cellular damage and inflammatory responses 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Oxygen-glucose deprivation (OGD) is a critical model for studying hypoxic-ischemic cerebrovascular disease in vitro. This paper is to investigate the protection of OGD-induced cellular damage and inflammatory responses by OGD preconditioning in vitro, to provide a theoretical basis for OGD preconditioning to improve the prevention and prognosis of ischemic stroke. OGD or OGD preconditioning model was established by culturing the PC12 cell line in vitro, followed by further adding A23187 (calcium ion carrier) or CsA (calcium ion antagonist). Cell viability was detected by MTT, apoptosis by Hoechst 33,258 staining, the levels of TNF-α and IL-1β mRNA by RT-qPCR and ELISA, and the levels of CaN, NFAT, COX-2 by RT-qPCR and Western blot. Cell viability was decreased, and apoptosis, inflammatory cytokines, and CaN, NFAT, and COX-2 levels were notably increased upon OGD, while OGD pretreatment significantly increased cell viability and decreased apoptosis, inflammation, and the Ca2+/CaN/NFAT pathway. Treatment with A23187 decreased cell viability, promoted apoptosis, and significantly increased TNF-α, IL-1β, CaN, NFAT, and COX-2 levels, while CsA treatment reduced the opposite results. In vitro OGD preconditioning mediates the Ca2+/CaN/NFAT pathway to protect against OGD-induced cellular damage and inflammatory responses. Oxygen-glucose deprivation Oxygen-glucose deprivation preconditioning Ca2+/CaN/NFAT pathway Cell viability Apoptosis Inflammatory factors Guo, Qingzi verfasserin aut An, Ran verfasserin aut Shen, Shuhan verfasserin aut Yin, Lin verfasserin (orcid)0009-0008-8711-4188 aut Enthalten in Brain research Amsterdam : Elsevier, 1966 1826 Online-Ressource (DE-627)254635776 (DE-600)1462674-3 (DE-576)074530976 1872-6240 nnns volume:1826 GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 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_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 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_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 Neurologie VZ AR 1826
allfieldsGer	10.1016/j.brainres.2023.148736 doi (DE-627)ELV066998611 (ELSEVIER)S0006-8993(23)00507-3 DE-627 ger DE-627 rda eng 150 610 VZ 44.90 bkl Zhang, Lihong verfasserin aut In vitro ischemic preconditioning mediates the Ca 2+ /CaN/NFAT pathway to protect against oxygen-glucose deprivation-induced cellular damage and inflammatory responses 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Oxygen-glucose deprivation (OGD) is a critical model for studying hypoxic-ischemic cerebrovascular disease in vitro. This paper is to investigate the protection of OGD-induced cellular damage and inflammatory responses by OGD preconditioning in vitro, to provide a theoretical basis for OGD preconditioning to improve the prevention and prognosis of ischemic stroke. OGD or OGD preconditioning model was established by culturing the PC12 cell line in vitro, followed by further adding A23187 (calcium ion carrier) or CsA (calcium ion antagonist). Cell viability was detected by MTT, apoptosis by Hoechst 33,258 staining, the levels of TNF-α and IL-1β mRNA by RT-qPCR and ELISA, and the levels of CaN, NFAT, COX-2 by RT-qPCR and Western blot. Cell viability was decreased, and apoptosis, inflammatory cytokines, and CaN, NFAT, and COX-2 levels were notably increased upon OGD, while OGD pretreatment significantly increased cell viability and decreased apoptosis, inflammation, and the Ca2+/CaN/NFAT pathway. Treatment with A23187 decreased cell viability, promoted apoptosis, and significantly increased TNF-α, IL-1β, CaN, NFAT, and COX-2 levels, while CsA treatment reduced the opposite results. In vitro OGD preconditioning mediates the Ca2+/CaN/NFAT pathway to protect against OGD-induced cellular damage and inflammatory responses. Oxygen-glucose deprivation Oxygen-glucose deprivation preconditioning Ca2+/CaN/NFAT pathway Cell viability Apoptosis Inflammatory factors Guo, Qingzi verfasserin aut An, Ran verfasserin aut Shen, Shuhan verfasserin aut Yin, Lin verfasserin (orcid)0009-0008-8711-4188 aut Enthalten in Brain research Amsterdam : Elsevier, 1966 1826 Online-Ressource (DE-627)254635776 (DE-600)1462674-3 (DE-576)074530976 1872-6240 nnns volume:1826 GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 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_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 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_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 Neurologie VZ AR 1826
allfieldsSound	10.1016/j.brainres.2023.148736 doi (DE-627)ELV066998611 (ELSEVIER)S0006-8993(23)00507-3 DE-627 ger DE-627 rda eng 150 610 VZ 44.90 bkl Zhang, Lihong verfasserin aut In vitro ischemic preconditioning mediates the Ca 2+ /CaN/NFAT pathway to protect against oxygen-glucose deprivation-induced cellular damage and inflammatory responses 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Oxygen-glucose deprivation (OGD) is a critical model for studying hypoxic-ischemic cerebrovascular disease in vitro. This paper is to investigate the protection of OGD-induced cellular damage and inflammatory responses by OGD preconditioning in vitro, to provide a theoretical basis for OGD preconditioning to improve the prevention and prognosis of ischemic stroke. OGD or OGD preconditioning model was established by culturing the PC12 cell line in vitro, followed by further adding A23187 (calcium ion carrier) or CsA (calcium ion antagonist). Cell viability was detected by MTT, apoptosis by Hoechst 33,258 staining, the levels of TNF-α and IL-1β mRNA by RT-qPCR and ELISA, and the levels of CaN, NFAT, COX-2 by RT-qPCR and Western blot. Cell viability was decreased, and apoptosis, inflammatory cytokines, and CaN, NFAT, and COX-2 levels were notably increased upon OGD, while OGD pretreatment significantly increased cell viability and decreased apoptosis, inflammation, and the Ca2+/CaN/NFAT pathway. Treatment with A23187 decreased cell viability, promoted apoptosis, and significantly increased TNF-α, IL-1β, CaN, NFAT, and COX-2 levels, while CsA treatment reduced the opposite results. In vitro OGD preconditioning mediates the Ca2+/CaN/NFAT pathway to protect against OGD-induced cellular damage and inflammatory responses. Oxygen-glucose deprivation Oxygen-glucose deprivation preconditioning Ca2+/CaN/NFAT pathway Cell viability Apoptosis Inflammatory factors Guo, Qingzi verfasserin aut An, Ran verfasserin aut Shen, Shuhan verfasserin aut Yin, Lin verfasserin (orcid)0009-0008-8711-4188 aut Enthalten in Brain research Amsterdam : Elsevier, 1966 1826 Online-Ressource (DE-627)254635776 (DE-600)1462674-3 (DE-576)074530976 1872-6240 nnns volume:1826 GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 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_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2088 GBV_ILN_2106 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2507 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 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_4338 GBV_ILN_4393 GBV_ILN_4700 44.90 Neurologie VZ AR 1826
language	English
source	Enthalten in Brain research 1826 volume:1826
sourceStr	Enthalten in Brain research 1826 volume:1826
format_phy_str_mv	Article
bklname	Neurologie
institution	findex.gbv.de
topic_facet	Oxygen-glucose deprivation Oxygen-glucose deprivation preconditioning Ca2+/CaN/NFAT pathway Cell viability Apoptosis Inflammatory factors
dewey-raw	150
isfreeaccess_bool	false
container_title	Brain research
authorswithroles_txt_mv	Zhang, Lihong @@aut@@ Guo, Qingzi @@aut@@ An, Ran @@aut@@ Shen, Shuhan @@aut@@ Yin, Lin @@aut@@
publishDateDaySort_date	2023-01-01T00:00:00Z
hierarchy_top_id	254635776
dewey-sort	3150
id	ELV066998611
language_de	englisch
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author	Zhang, Lihong
spellingShingle	Zhang, Lihong ddc 150 bkl 44.90 misc Oxygen-glucose deprivation misc Oxygen-glucose deprivation preconditioning misc Ca2+/CaN/NFAT pathway misc Cell viability misc Apoptosis misc Inflammatory factors In vitro ischemic preconditioning mediates the Ca 2+ /CaN/NFAT pathway to protect against oxygen-glucose deprivation-induced cellular damage and inflammatory responses
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topic_title	150 610 VZ 44.90 bkl In vitro ischemic preconditioning mediates the Ca 2+ /CaN/NFAT pathway to protect against oxygen-glucose deprivation-induced cellular damage and inflammatory responses Oxygen-glucose deprivation Oxygen-glucose deprivation preconditioning Ca2+/CaN/NFAT pathway Cell viability Apoptosis Inflammatory factors
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title	In vitro ischemic preconditioning mediates the Ca 2+ /CaN/NFAT pathway to protect against oxygen-glucose deprivation-induced cellular damage and inflammatory responses
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title_full	In vitro ischemic preconditioning mediates the Ca 2+ /CaN/NFAT pathway to protect against oxygen-glucose deprivation-induced cellular damage and inflammatory responses
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title_sort	in vitro ischemic preconditioning mediates the ca 2+ /can/nfat pathway to protect against oxygen-glucose deprivation-induced cellular damage and inflammatory responses
title_auth	In vitro ischemic preconditioning mediates the Ca 2+ /CaN/NFAT pathway to protect against oxygen-glucose deprivation-induced cellular damage and inflammatory responses
abstract	Oxygen-glucose deprivation (OGD) is a critical model for studying hypoxic-ischemic cerebrovascular disease in vitro. This paper is to investigate the protection of OGD-induced cellular damage and inflammatory responses by OGD preconditioning in vitro, to provide a theoretical basis for OGD preconditioning to improve the prevention and prognosis of ischemic stroke. OGD or OGD preconditioning model was established by culturing the PC12 cell line in vitro, followed by further adding A23187 (calcium ion carrier) or CsA (calcium ion antagonist). Cell viability was detected by MTT, apoptosis by Hoechst 33,258 staining, the levels of TNF-α and IL-1β mRNA by RT-qPCR and ELISA, and the levels of CaN, NFAT, COX-2 by RT-qPCR and Western blot. Cell viability was decreased, and apoptosis, inflammatory cytokines, and CaN, NFAT, and COX-2 levels were notably increased upon OGD, while OGD pretreatment significantly increased cell viability and decreased apoptosis, inflammation, and the Ca2+/CaN/NFAT pathway. Treatment with A23187 decreased cell viability, promoted apoptosis, and significantly increased TNF-α, IL-1β, CaN, NFAT, and COX-2 levels, while CsA treatment reduced the opposite results. In vitro OGD preconditioning mediates the Ca2+/CaN/NFAT pathway to protect against OGD-induced cellular damage and inflammatory responses.
abstractGer	Oxygen-glucose deprivation (OGD) is a critical model for studying hypoxic-ischemic cerebrovascular disease in vitro. This paper is to investigate the protection of OGD-induced cellular damage and inflammatory responses by OGD preconditioning in vitro, to provide a theoretical basis for OGD preconditioning to improve the prevention and prognosis of ischemic stroke. OGD or OGD preconditioning model was established by culturing the PC12 cell line in vitro, followed by further adding A23187 (calcium ion carrier) or CsA (calcium ion antagonist). Cell viability was detected by MTT, apoptosis by Hoechst 33,258 staining, the levels of TNF-α and IL-1β mRNA by RT-qPCR and ELISA, and the levels of CaN, NFAT, COX-2 by RT-qPCR and Western blot. Cell viability was decreased, and apoptosis, inflammatory cytokines, and CaN, NFAT, and COX-2 levels were notably increased upon OGD, while OGD pretreatment significantly increased cell viability and decreased apoptosis, inflammation, and the Ca2+/CaN/NFAT pathway. Treatment with A23187 decreased cell viability, promoted apoptosis, and significantly increased TNF-α, IL-1β, CaN, NFAT, and COX-2 levels, while CsA treatment reduced the opposite results. In vitro OGD preconditioning mediates the Ca2+/CaN/NFAT pathway to protect against OGD-induced cellular damage and inflammatory responses.
abstract_unstemmed	Oxygen-glucose deprivation (OGD) is a critical model for studying hypoxic-ischemic cerebrovascular disease in vitro. This paper is to investigate the protection of OGD-induced cellular damage and inflammatory responses by OGD preconditioning in vitro, to provide a theoretical basis for OGD preconditioning to improve the prevention and prognosis of ischemic stroke. OGD or OGD preconditioning model was established by culturing the PC12 cell line in vitro, followed by further adding A23187 (calcium ion carrier) or CsA (calcium ion antagonist). Cell viability was detected by MTT, apoptosis by Hoechst 33,258 staining, the levels of TNF-α and IL-1β mRNA by RT-qPCR and ELISA, and the levels of CaN, NFAT, COX-2 by RT-qPCR and Western blot. Cell viability was decreased, and apoptosis, inflammatory cytokines, and CaN, NFAT, and COX-2 levels were notably increased upon OGD, while OGD pretreatment significantly increased cell viability and decreased apoptosis, inflammation, and the Ca2+/CaN/NFAT pathway. Treatment with A23187 decreased cell viability, promoted apoptosis, and significantly increased TNF-α, IL-1β, CaN, NFAT, and COX-2 levels, while CsA treatment reduced the opposite results. In vitro OGD preconditioning mediates the Ca2+/CaN/NFAT pathway to protect against OGD-induced cellular damage and inflammatory responses.
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title_short	In vitro ischemic preconditioning mediates the Ca 2+ /CaN/NFAT pathway to protect against oxygen-glucose deprivation-induced cellular damage and inflammatory responses
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In vitro ischemic preconditioning mediates the Ca 2+ /CaN/NFAT pathway to protect against oxygen-glucose deprivation-induced cellular damage and inflammatory responses

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