Hydroxychloroquine alleviates the neurotoxicity induced by anti-ribosomal P antibodies

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by a wide spectrum of autoantibodies, among which anti-ribosomal P (anti-P) antibodies are considered to be closely related to the neuropsychiatric SLE (NPSLE). Hydroxychloroquine (HCQ) has been proven to be effective a...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Zhao, Xinnan [verfasserIn] Yang, Pingting [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	Anti-ribosomal P antibodies Hydroxychloroquine Systemic lupus erythematosus Neuropsychiatric systemic lupus erythematosus Neurotoxicity

Übergeordnetes Werk:	Enthalten in: Journal of neuroimmunology - Amsterdam [u.a.] : Elsevier Science, 1981, 358
Übergeordnetes Werk:	volume:358

DOI / URN:	10.1016/j.jneuroim.2021.577648

Katalog-ID:	ELV006361420

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245	1	0	\|a Hydroxychloroquine alleviates the neurotoxicity induced by anti-ribosomal P antibodies
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520			\|a Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by a wide spectrum of autoantibodies, among which anti-ribosomal P (anti-P) antibodies are considered to be closely related to the neuropsychiatric SLE (NPSLE). Hydroxychloroquine (HCQ) has been proven to be effective against a variety of autoimmune diseases and is an essential drug for the treatment of SLE. In this study, we investigated the effects of anti-ribosomal P (anti-P) antibodies on neural cells and determined whether hydroxychloroquine (HCQ) influenced the anti-P antibodies-induced changes. The results showed that the binding of anti-P antibodies with mouse neuroblastoma- 2a (N2a) cells and rat primary neurons resulted in elevated intracellular calcium levels, inducing decreased cell viability and cell apoptosis. These inhibitory effects were alleviated by HCQ in a concentration-dependent manner by reducing the intracellular calcium levels and modulating the expression of apoptotic proteins. In summary, our study demonstrates that anti-P antibodies induce neural cell damage. HCQ could ease the damage effects and may play a neuroprotective role in NPSLE.
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650		4	\|a Hydroxychloroquine
650		4	\|a Systemic lupus erythematosus
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650		4	\|a Neurotoxicity
700	1		\|a Yang, Pingting \|e verfasserin \|4 aut
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Indexfelder

author_variant	x z xz p y py
matchkey_str	article:18728421:2021----::yrxclrqieleitshnuooiiynuebat
hierarchy_sort_str	2021
bklnumber	44.90 44.45
publishDate	2021
allfields	10.1016/j.jneuroim.2021.577648 doi (DE-627)ELV006361420 (ELSEVIER)S0165-5728(21)00175-2 DE-627 ger DE-627 rda eng 610 DE-600 44.90 bkl 44.45 bkl Zhao, Xinnan verfasserin aut Hydroxychloroquine alleviates the neurotoxicity induced by anti-ribosomal P antibodies 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by a wide spectrum of autoantibodies, among which anti-ribosomal P (anti-P) antibodies are considered to be closely related to the neuropsychiatric SLE (NPSLE). Hydroxychloroquine (HCQ) has been proven to be effective against a variety of autoimmune diseases and is an essential drug for the treatment of SLE. In this study, we investigated the effects of anti-ribosomal P (anti-P) antibodies on neural cells and determined whether hydroxychloroquine (HCQ) influenced the anti-P antibodies-induced changes. The results showed that the binding of anti-P antibodies with mouse neuroblastoma- 2a (N2a) cells and rat primary neurons resulted in elevated intracellular calcium levels, inducing decreased cell viability and cell apoptosis. These inhibitory effects were alleviated by HCQ in a concentration-dependent manner by reducing the intracellular calcium levels and modulating the expression of apoptotic proteins. In summary, our study demonstrates that anti-P antibodies induce neural cell damage. HCQ could ease the damage effects and may play a neuroprotective role in NPSLE. Anti-ribosomal P antibodies Hydroxychloroquine Systemic lupus erythematosus Neuropsychiatric systemic lupus erythematosus Neurotoxicity Yang, Pingting verfasserin aut Enthalten in Journal of neuroimmunology Amsterdam [u.a.] : Elsevier Science, 1981 358 Online-Ressource (DE-627)306659778 (DE-600)1500497-1 (DE-576)081986408 1872-8421 nnns volume:358 GBV_USEFLAG_U SYSFLAG_U GBV_ELV 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_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_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.90 Neurologie 44.45 Immunologie AR 358
spelling	10.1016/j.jneuroim.2021.577648 doi (DE-627)ELV006361420 (ELSEVIER)S0165-5728(21)00175-2 DE-627 ger DE-627 rda eng 610 DE-600 44.90 bkl 44.45 bkl Zhao, Xinnan verfasserin aut Hydroxychloroquine alleviates the neurotoxicity induced by anti-ribosomal P antibodies 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by a wide spectrum of autoantibodies, among which anti-ribosomal P (anti-P) antibodies are considered to be closely related to the neuropsychiatric SLE (NPSLE). Hydroxychloroquine (HCQ) has been proven to be effective against a variety of autoimmune diseases and is an essential drug for the treatment of SLE. In this study, we investigated the effects of anti-ribosomal P (anti-P) antibodies on neural cells and determined whether hydroxychloroquine (HCQ) influenced the anti-P antibodies-induced changes. The results showed that the binding of anti-P antibodies with mouse neuroblastoma- 2a (N2a) cells and rat primary neurons resulted in elevated intracellular calcium levels, inducing decreased cell viability and cell apoptosis. These inhibitory effects were alleviated by HCQ in a concentration-dependent manner by reducing the intracellular calcium levels and modulating the expression of apoptotic proteins. In summary, our study demonstrates that anti-P antibodies induce neural cell damage. HCQ could ease the damage effects and may play a neuroprotective role in NPSLE. Anti-ribosomal P antibodies Hydroxychloroquine Systemic lupus erythematosus Neuropsychiatric systemic lupus erythematosus Neurotoxicity Yang, Pingting verfasserin aut Enthalten in Journal of neuroimmunology Amsterdam [u.a.] : Elsevier Science, 1981 358 Online-Ressource (DE-627)306659778 (DE-600)1500497-1 (DE-576)081986408 1872-8421 nnns volume:358 GBV_USEFLAG_U SYSFLAG_U GBV_ELV 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_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_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.90 Neurologie 44.45 Immunologie AR 358
allfields_unstemmed	10.1016/j.jneuroim.2021.577648 doi (DE-627)ELV006361420 (ELSEVIER)S0165-5728(21)00175-2 DE-627 ger DE-627 rda eng 610 DE-600 44.90 bkl 44.45 bkl Zhao, Xinnan verfasserin aut Hydroxychloroquine alleviates the neurotoxicity induced by anti-ribosomal P antibodies 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by a wide spectrum of autoantibodies, among which anti-ribosomal P (anti-P) antibodies are considered to be closely related to the neuropsychiatric SLE (NPSLE). Hydroxychloroquine (HCQ) has been proven to be effective against a variety of autoimmune diseases and is an essential drug for the treatment of SLE. In this study, we investigated the effects of anti-ribosomal P (anti-P) antibodies on neural cells and determined whether hydroxychloroquine (HCQ) influenced the anti-P antibodies-induced changes. The results showed that the binding of anti-P antibodies with mouse neuroblastoma- 2a (N2a) cells and rat primary neurons resulted in elevated intracellular calcium levels, inducing decreased cell viability and cell apoptosis. These inhibitory effects were alleviated by HCQ in a concentration-dependent manner by reducing the intracellular calcium levels and modulating the expression of apoptotic proteins. In summary, our study demonstrates that anti-P antibodies induce neural cell damage. HCQ could ease the damage effects and may play a neuroprotective role in NPSLE. Anti-ribosomal P antibodies Hydroxychloroquine Systemic lupus erythematosus Neuropsychiatric systemic lupus erythematosus Neurotoxicity Yang, Pingting verfasserin aut Enthalten in Journal of neuroimmunology Amsterdam [u.a.] : Elsevier Science, 1981 358 Online-Ressource (DE-627)306659778 (DE-600)1500497-1 (DE-576)081986408 1872-8421 nnns volume:358 GBV_USEFLAG_U SYSFLAG_U GBV_ELV 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_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_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.90 Neurologie 44.45 Immunologie AR 358
allfieldsGer	10.1016/j.jneuroim.2021.577648 doi (DE-627)ELV006361420 (ELSEVIER)S0165-5728(21)00175-2 DE-627 ger DE-627 rda eng 610 DE-600 44.90 bkl 44.45 bkl Zhao, Xinnan verfasserin aut Hydroxychloroquine alleviates the neurotoxicity induced by anti-ribosomal P antibodies 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by a wide spectrum of autoantibodies, among which anti-ribosomal P (anti-P) antibodies are considered to be closely related to the neuropsychiatric SLE (NPSLE). Hydroxychloroquine (HCQ) has been proven to be effective against a variety of autoimmune diseases and is an essential drug for the treatment of SLE. In this study, we investigated the effects of anti-ribosomal P (anti-P) antibodies on neural cells and determined whether hydroxychloroquine (HCQ) influenced the anti-P antibodies-induced changes. The results showed that the binding of anti-P antibodies with mouse neuroblastoma- 2a (N2a) cells and rat primary neurons resulted in elevated intracellular calcium levels, inducing decreased cell viability and cell apoptosis. These inhibitory effects were alleviated by HCQ in a concentration-dependent manner by reducing the intracellular calcium levels and modulating the expression of apoptotic proteins. In summary, our study demonstrates that anti-P antibodies induce neural cell damage. HCQ could ease the damage effects and may play a neuroprotective role in NPSLE. Anti-ribosomal P antibodies Hydroxychloroquine Systemic lupus erythematosus Neuropsychiatric systemic lupus erythematosus Neurotoxicity Yang, Pingting verfasserin aut Enthalten in Journal of neuroimmunology Amsterdam [u.a.] : Elsevier Science, 1981 358 Online-Ressource (DE-627)306659778 (DE-600)1500497-1 (DE-576)081986408 1872-8421 nnns volume:358 GBV_USEFLAG_U SYSFLAG_U GBV_ELV 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_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_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.90 Neurologie 44.45 Immunologie AR 358
allfieldsSound	10.1016/j.jneuroim.2021.577648 doi (DE-627)ELV006361420 (ELSEVIER)S0165-5728(21)00175-2 DE-627 ger DE-627 rda eng 610 DE-600 44.90 bkl 44.45 bkl Zhao, Xinnan verfasserin aut Hydroxychloroquine alleviates the neurotoxicity induced by anti-ribosomal P antibodies 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by a wide spectrum of autoantibodies, among which anti-ribosomal P (anti-P) antibodies are considered to be closely related to the neuropsychiatric SLE (NPSLE). Hydroxychloroquine (HCQ) has been proven to be effective against a variety of autoimmune diseases and is an essential drug for the treatment of SLE. In this study, we investigated the effects of anti-ribosomal P (anti-P) antibodies on neural cells and determined whether hydroxychloroquine (HCQ) influenced the anti-P antibodies-induced changes. The results showed that the binding of anti-P antibodies with mouse neuroblastoma- 2a (N2a) cells and rat primary neurons resulted in elevated intracellular calcium levels, inducing decreased cell viability and cell apoptosis. These inhibitory effects were alleviated by HCQ in a concentration-dependent manner by reducing the intracellular calcium levels and modulating the expression of apoptotic proteins. In summary, our study demonstrates that anti-P antibodies induce neural cell damage. HCQ could ease the damage effects and may play a neuroprotective role in NPSLE. Anti-ribosomal P antibodies Hydroxychloroquine Systemic lupus erythematosus Neuropsychiatric systemic lupus erythematosus Neurotoxicity Yang, Pingting verfasserin aut Enthalten in Journal of neuroimmunology Amsterdam [u.a.] : Elsevier Science, 1981 358 Online-Ressource (DE-627)306659778 (DE-600)1500497-1 (DE-576)081986408 1872-8421 nnns volume:358 GBV_USEFLAG_U SYSFLAG_U GBV_ELV 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_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_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2056 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2336 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4313 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4393 44.90 Neurologie 44.45 Immunologie AR 358
language	English
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author	Zhao, Xinnan
spellingShingle	Zhao, Xinnan ddc 610 bkl 44.90 bkl 44.45 misc Anti-ribosomal P antibodies misc Hydroxychloroquine misc Systemic lupus erythematosus misc Neuropsychiatric systemic lupus erythematosus misc Neurotoxicity Hydroxychloroquine alleviates the neurotoxicity induced by anti-ribosomal P antibodies
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topic_title	610 DE-600 44.90 bkl 44.45 bkl Hydroxychloroquine alleviates the neurotoxicity induced by anti-ribosomal P antibodies Anti-ribosomal P antibodies Hydroxychloroquine Systemic lupus erythematosus Neuropsychiatric systemic lupus erythematosus Neurotoxicity
topic	ddc 610 bkl 44.90 bkl 44.45 misc Anti-ribosomal P antibodies misc Hydroxychloroquine misc Systemic lupus erythematosus misc Neuropsychiatric systemic lupus erythematosus misc Neurotoxicity
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title	Hydroxychloroquine alleviates the neurotoxicity induced by anti-ribosomal P antibodies
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title_full	Hydroxychloroquine alleviates the neurotoxicity induced by anti-ribosomal P antibodies
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title_sort	hydroxychloroquine alleviates the neurotoxicity induced by anti-ribosomal p antibodies
title_auth	Hydroxychloroquine alleviates the neurotoxicity induced by anti-ribosomal P antibodies
abstract	Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by a wide spectrum of autoantibodies, among which anti-ribosomal P (anti-P) antibodies are considered to be closely related to the neuropsychiatric SLE (NPSLE). Hydroxychloroquine (HCQ) has been proven to be effective against a variety of autoimmune diseases and is an essential drug for the treatment of SLE. In this study, we investigated the effects of anti-ribosomal P (anti-P) antibodies on neural cells and determined whether hydroxychloroquine (HCQ) influenced the anti-P antibodies-induced changes. The results showed that the binding of anti-P antibodies with mouse neuroblastoma- 2a (N2a) cells and rat primary neurons resulted in elevated intracellular calcium levels, inducing decreased cell viability and cell apoptosis. These inhibitory effects were alleviated by HCQ in a concentration-dependent manner by reducing the intracellular calcium levels and modulating the expression of apoptotic proteins. In summary, our study demonstrates that anti-P antibodies induce neural cell damage. HCQ could ease the damage effects and may play a neuroprotective role in NPSLE.
abstractGer	Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by a wide spectrum of autoantibodies, among which anti-ribosomal P (anti-P) antibodies are considered to be closely related to the neuropsychiatric SLE (NPSLE). Hydroxychloroquine (HCQ) has been proven to be effective against a variety of autoimmune diseases and is an essential drug for the treatment of SLE. In this study, we investigated the effects of anti-ribosomal P (anti-P) antibodies on neural cells and determined whether hydroxychloroquine (HCQ) influenced the anti-P antibodies-induced changes. The results showed that the binding of anti-P antibodies with mouse neuroblastoma- 2a (N2a) cells and rat primary neurons resulted in elevated intracellular calcium levels, inducing decreased cell viability and cell apoptosis. These inhibitory effects were alleviated by HCQ in a concentration-dependent manner by reducing the intracellular calcium levels and modulating the expression of apoptotic proteins. In summary, our study demonstrates that anti-P antibodies induce neural cell damage. HCQ could ease the damage effects and may play a neuroprotective role in NPSLE.
abstract_unstemmed	Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by a wide spectrum of autoantibodies, among which anti-ribosomal P (anti-P) antibodies are considered to be closely related to the neuropsychiatric SLE (NPSLE). Hydroxychloroquine (HCQ) has been proven to be effective against a variety of autoimmune diseases and is an essential drug for the treatment of SLE. In this study, we investigated the effects of anti-ribosomal P (anti-P) antibodies on neural cells and determined whether hydroxychloroquine (HCQ) influenced the anti-P antibodies-induced changes. The results showed that the binding of anti-P antibodies with mouse neuroblastoma- 2a (N2a) cells and rat primary neurons resulted in elevated intracellular calcium levels, inducing decreased cell viability and cell apoptosis. These inhibitory effects were alleviated by HCQ in a concentration-dependent manner by reducing the intracellular calcium levels and modulating the expression of apoptotic proteins. In summary, our study demonstrates that anti-P antibodies induce neural cell damage. HCQ could ease the damage effects and may play a neuroprotective role in NPSLE.
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title_short	Hydroxychloroquine alleviates the neurotoxicity induced by anti-ribosomal P antibodies
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up_date	2024-07-06T21:07:13.410Z
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fullrecord_marcxml	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV006361420</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230524160534.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230505s2021 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.jneuroim.2021.577648</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV006361420</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0165-5728(21)00175-2</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rda</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.90</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.45</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Zhao, Xinnan</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Hydroxychloroquine alleviates the neurotoxicity induced by anti-ribosomal P antibodies</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2021</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by a wide spectrum of autoantibodies, among which anti-ribosomal P (anti-P) antibodies are considered to be closely related to the neuropsychiatric SLE (NPSLE). Hydroxychloroquine (HCQ) has been proven to be effective against a variety of autoimmune diseases and is an essential drug for the treatment of SLE. In this study, we investigated the effects of anti-ribosomal P (anti-P) antibodies on neural cells and determined whether hydroxychloroquine (HCQ) influenced the anti-P antibodies-induced changes. The results showed that the binding of anti-P antibodies with mouse neuroblastoma- 2a (N2a) cells and rat primary neurons resulted in elevated intracellular calcium levels, inducing decreased cell viability and cell apoptosis. These inhibitory effects were alleviated by HCQ in a concentration-dependent manner by reducing the intracellular calcium levels and modulating the expression of apoptotic proteins. In summary, our study demonstrates that anti-P antibodies induce neural cell damage. 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Hydroxychloroquine alleviates the neurotoxicity induced by anti-ribosomal P antibodies

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