Inhibition of glycolysis prevents behavioural changes in mice with MK801-induced SCZ model by alleviating lactate accumulation and lactylation

Schizophrenia (SCZ) is a debilitating neuropsychiatric disorder with a complex aetiology. Cognitive symptoms and hippocampal changes have been implicated in the pathophysiology of SCZ. Changes in metabolites level and up-regulated glycolysis have been reported in previous studies, which may be relat...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Xie, Jiming [verfasserIn] Hong, Shijun [verfasserIn] Zhang, Xiufeng [verfasserIn] Li, Yuwen [verfasserIn] Xie, Runfang [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	Schizophrenia Hippocampal neurons Glycolysis Lactylation HMGB1

Übergeordnetes Werk:	Enthalten in: Brain research - Amsterdam : Elsevier, 1966, 1812
Übergeordnetes Werk:	volume:1812

DOI / URN:	10.1016/j.brainres.2023.148409

Katalog-ID:	ELV010073647

Internformat


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245	1	0	\|a Inhibition of glycolysis prevents behavioural changes in mice with MK801-induced SCZ model by alleviating lactate accumulation and lactylation
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520			\|a Schizophrenia (SCZ) is a debilitating neuropsychiatric disorder with a complex aetiology. Cognitive symptoms and hippocampal changes have been implicated in the pathophysiology of SCZ. Changes in metabolites level and up-regulated glycolysis have been reported in previous studies, which may be related to the hippocampal dysfunction in SCZ. However, the pathological mechanism of glycolysis involved in the pathogenesis of SCZ remains unclear. Therefore, the change of glycolysis level and the involvement in SCZ need to be further studied. In our study, MK801 was used to induce an SCZ mouse model and cell model in vivo and in vitro. Western blotting was performed to evaluate the levels of glycolysis, metabolites, and lactylation in hippocampal tissue of mice with SCZ or cell models. The level of high mobility group protein 1 (HMGB1) in the medium of MK801-treated primary hippocampal neurons was examined. Apoptosis was evaluated in HMGB1-treated hippocampal neurons by flow cytometry. The glycolysis inhibitor 2-DG prevented behavioural changes in the MK801-induced SCZ mouse model. The lactate accumulation and level of lactylation were alleviated in the hippocampal tissue of MK801-treated mice. Glycolysis was enhanced, and lactate accumulated in MK-801-treated primary hippocampal neurons. In addition, the level of HMGB1 increased in the medium and induced apoptosis in primary hippocampal neurons. Together, the data showed that glycolysis and lactylation increased in the MK801-induced SCZ model in vivo and in vitro, and this effect could be prevented by 2-DG (a glycolysis inhibitor). Glycolytic related HMGB1 upregulation may induce apoptosis in hippocampal neurons downstream.
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publishDate	2023
allfields	10.1016/j.brainres.2023.148409 doi (DE-627)ELV010073647 (ELSEVIER)S0006-8993(23)00180-4 DE-627 ger DE-627 rda eng 150 610 VZ 44.90 bkl Xie, Jiming verfasserin aut Inhibition of glycolysis prevents behavioural changes in mice with MK801-induced SCZ model by alleviating lactate accumulation and lactylation 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Schizophrenia (SCZ) is a debilitating neuropsychiatric disorder with a complex aetiology. Cognitive symptoms and hippocampal changes have been implicated in the pathophysiology of SCZ. Changes in metabolites level and up-regulated glycolysis have been reported in previous studies, which may be related to the hippocampal dysfunction in SCZ. However, the pathological mechanism of glycolysis involved in the pathogenesis of SCZ remains unclear. Therefore, the change of glycolysis level and the involvement in SCZ need to be further studied. In our study, MK801 was used to induce an SCZ mouse model and cell model in vivo and in vitro. Western blotting was performed to evaluate the levels of glycolysis, metabolites, and lactylation in hippocampal tissue of mice with SCZ or cell models. The level of high mobility group protein 1 (HMGB1) in the medium of MK801-treated primary hippocampal neurons was examined. Apoptosis was evaluated in HMGB1-treated hippocampal neurons by flow cytometry. The glycolysis inhibitor 2-DG prevented behavioural changes in the MK801-induced SCZ mouse model. The lactate accumulation and level of lactylation were alleviated in the hippocampal tissue of MK801-treated mice. Glycolysis was enhanced, and lactate accumulated in MK-801-treated primary hippocampal neurons. In addition, the level of HMGB1 increased in the medium and induced apoptosis in primary hippocampal neurons. Together, the data showed that glycolysis and lactylation increased in the MK801-induced SCZ model in vivo and in vitro, and this effect could be prevented by 2-DG (a glycolysis inhibitor). Glycolytic related HMGB1 upregulation may induce apoptosis in hippocampal neurons downstream. Schizophrenia Hippocampal neurons Glycolysis Lactylation HMGB1 Hong, Shijun verfasserin aut Zhang, Xiufeng verfasserin aut Li, Yuwen verfasserin aut Xie, Runfang verfasserin aut Enthalten in Brain research Amsterdam : Elsevier, 1966 1812 Online-Ressource (DE-627)254635776 (DE-600)1462674-3 (DE-576)074530976 1872-6240 nnns volume:1812 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_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 1812
spelling	10.1016/j.brainres.2023.148409 doi (DE-627)ELV010073647 (ELSEVIER)S0006-8993(23)00180-4 DE-627 ger DE-627 rda eng 150 610 VZ 44.90 bkl Xie, Jiming verfasserin aut Inhibition of glycolysis prevents behavioural changes in mice with MK801-induced SCZ model by alleviating lactate accumulation and lactylation 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Schizophrenia (SCZ) is a debilitating neuropsychiatric disorder with a complex aetiology. Cognitive symptoms and hippocampal changes have been implicated in the pathophysiology of SCZ. Changes in metabolites level and up-regulated glycolysis have been reported in previous studies, which may be related to the hippocampal dysfunction in SCZ. However, the pathological mechanism of glycolysis involved in the pathogenesis of SCZ remains unclear. Therefore, the change of glycolysis level and the involvement in SCZ need to be further studied. In our study, MK801 was used to induce an SCZ mouse model and cell model in vivo and in vitro. Western blotting was performed to evaluate the levels of glycolysis, metabolites, and lactylation in hippocampal tissue of mice with SCZ or cell models. The level of high mobility group protein 1 (HMGB1) in the medium of MK801-treated primary hippocampal neurons was examined. Apoptosis was evaluated in HMGB1-treated hippocampal neurons by flow cytometry. The glycolysis inhibitor 2-DG prevented behavioural changes in the MK801-induced SCZ mouse model. The lactate accumulation and level of lactylation were alleviated in the hippocampal tissue of MK801-treated mice. Glycolysis was enhanced, and lactate accumulated in MK-801-treated primary hippocampal neurons. In addition, the level of HMGB1 increased in the medium and induced apoptosis in primary hippocampal neurons. Together, the data showed that glycolysis and lactylation increased in the MK801-induced SCZ model in vivo and in vitro, and this effect could be prevented by 2-DG (a glycolysis inhibitor). Glycolytic related HMGB1 upregulation may induce apoptosis in hippocampal neurons downstream. Schizophrenia Hippocampal neurons Glycolysis Lactylation HMGB1 Hong, Shijun verfasserin aut Zhang, Xiufeng verfasserin aut Li, Yuwen verfasserin aut Xie, Runfang verfasserin aut Enthalten in Brain research Amsterdam : Elsevier, 1966 1812 Online-Ressource (DE-627)254635776 (DE-600)1462674-3 (DE-576)074530976 1872-6240 nnns volume:1812 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_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 1812
allfields_unstemmed	10.1016/j.brainres.2023.148409 doi (DE-627)ELV010073647 (ELSEVIER)S0006-8993(23)00180-4 DE-627 ger DE-627 rda eng 150 610 VZ 44.90 bkl Xie, Jiming verfasserin aut Inhibition of glycolysis prevents behavioural changes in mice with MK801-induced SCZ model by alleviating lactate accumulation and lactylation 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Schizophrenia (SCZ) is a debilitating neuropsychiatric disorder with a complex aetiology. Cognitive symptoms and hippocampal changes have been implicated in the pathophysiology of SCZ. Changes in metabolites level and up-regulated glycolysis have been reported in previous studies, which may be related to the hippocampal dysfunction in SCZ. However, the pathological mechanism of glycolysis involved in the pathogenesis of SCZ remains unclear. Therefore, the change of glycolysis level and the involvement in SCZ need to be further studied. In our study, MK801 was used to induce an SCZ mouse model and cell model in vivo and in vitro. Western blotting was performed to evaluate the levels of glycolysis, metabolites, and lactylation in hippocampal tissue of mice with SCZ or cell models. The level of high mobility group protein 1 (HMGB1) in the medium of MK801-treated primary hippocampal neurons was examined. Apoptosis was evaluated in HMGB1-treated hippocampal neurons by flow cytometry. The glycolysis inhibitor 2-DG prevented behavioural changes in the MK801-induced SCZ mouse model. The lactate accumulation and level of lactylation were alleviated in the hippocampal tissue of MK801-treated mice. Glycolysis was enhanced, and lactate accumulated in MK-801-treated primary hippocampal neurons. In addition, the level of HMGB1 increased in the medium and induced apoptosis in primary hippocampal neurons. Together, the data showed that glycolysis and lactylation increased in the MK801-induced SCZ model in vivo and in vitro, and this effect could be prevented by 2-DG (a glycolysis inhibitor). Glycolytic related HMGB1 upregulation may induce apoptosis in hippocampal neurons downstream. Schizophrenia Hippocampal neurons Glycolysis Lactylation HMGB1 Hong, Shijun verfasserin aut Zhang, Xiufeng verfasserin aut Li, Yuwen verfasserin aut Xie, Runfang verfasserin aut Enthalten in Brain research Amsterdam : Elsevier, 1966 1812 Online-Ressource (DE-627)254635776 (DE-600)1462674-3 (DE-576)074530976 1872-6240 nnns volume:1812 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_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 1812
allfieldsGer	10.1016/j.brainres.2023.148409 doi (DE-627)ELV010073647 (ELSEVIER)S0006-8993(23)00180-4 DE-627 ger DE-627 rda eng 150 610 VZ 44.90 bkl Xie, Jiming verfasserin aut Inhibition of glycolysis prevents behavioural changes in mice with MK801-induced SCZ model by alleviating lactate accumulation and lactylation 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Schizophrenia (SCZ) is a debilitating neuropsychiatric disorder with a complex aetiology. Cognitive symptoms and hippocampal changes have been implicated in the pathophysiology of SCZ. Changes in metabolites level and up-regulated glycolysis have been reported in previous studies, which may be related to the hippocampal dysfunction in SCZ. However, the pathological mechanism of glycolysis involved in the pathogenesis of SCZ remains unclear. Therefore, the change of glycolysis level and the involvement in SCZ need to be further studied. In our study, MK801 was used to induce an SCZ mouse model and cell model in vivo and in vitro. Western blotting was performed to evaluate the levels of glycolysis, metabolites, and lactylation in hippocampal tissue of mice with SCZ or cell models. The level of high mobility group protein 1 (HMGB1) in the medium of MK801-treated primary hippocampal neurons was examined. Apoptosis was evaluated in HMGB1-treated hippocampal neurons by flow cytometry. The glycolysis inhibitor 2-DG prevented behavioural changes in the MK801-induced SCZ mouse model. The lactate accumulation and level of lactylation were alleviated in the hippocampal tissue of MK801-treated mice. Glycolysis was enhanced, and lactate accumulated in MK-801-treated primary hippocampal neurons. In addition, the level of HMGB1 increased in the medium and induced apoptosis in primary hippocampal neurons. Together, the data showed that glycolysis and lactylation increased in the MK801-induced SCZ model in vivo and in vitro, and this effect could be prevented by 2-DG (a glycolysis inhibitor). Glycolytic related HMGB1 upregulation may induce apoptosis in hippocampal neurons downstream. Schizophrenia Hippocampal neurons Glycolysis Lactylation HMGB1 Hong, Shijun verfasserin aut Zhang, Xiufeng verfasserin aut Li, Yuwen verfasserin aut Xie, Runfang verfasserin aut Enthalten in Brain research Amsterdam : Elsevier, 1966 1812 Online-Ressource (DE-627)254635776 (DE-600)1462674-3 (DE-576)074530976 1872-6240 nnns volume:1812 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_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 1812
allfieldsSound	10.1016/j.brainres.2023.148409 doi (DE-627)ELV010073647 (ELSEVIER)S0006-8993(23)00180-4 DE-627 ger DE-627 rda eng 150 610 VZ 44.90 bkl Xie, Jiming verfasserin aut Inhibition of glycolysis prevents behavioural changes in mice with MK801-induced SCZ model by alleviating lactate accumulation and lactylation 2023 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Schizophrenia (SCZ) is a debilitating neuropsychiatric disorder with a complex aetiology. Cognitive symptoms and hippocampal changes have been implicated in the pathophysiology of SCZ. Changes in metabolites level and up-regulated glycolysis have been reported in previous studies, which may be related to the hippocampal dysfunction in SCZ. However, the pathological mechanism of glycolysis involved in the pathogenesis of SCZ remains unclear. Therefore, the change of glycolysis level and the involvement in SCZ need to be further studied. In our study, MK801 was used to induce an SCZ mouse model and cell model in vivo and in vitro. Western blotting was performed to evaluate the levels of glycolysis, metabolites, and lactylation in hippocampal tissue of mice with SCZ or cell models. The level of high mobility group protein 1 (HMGB1) in the medium of MK801-treated primary hippocampal neurons was examined. Apoptosis was evaluated in HMGB1-treated hippocampal neurons by flow cytometry. The glycolysis inhibitor 2-DG prevented behavioural changes in the MK801-induced SCZ mouse model. The lactate accumulation and level of lactylation were alleviated in the hippocampal tissue of MK801-treated mice. Glycolysis was enhanced, and lactate accumulated in MK-801-treated primary hippocampal neurons. In addition, the level of HMGB1 increased in the medium and induced apoptosis in primary hippocampal neurons. Together, the data showed that glycolysis and lactylation increased in the MK801-induced SCZ model in vivo and in vitro, and this effect could be prevented by 2-DG (a glycolysis inhibitor). Glycolytic related HMGB1 upregulation may induce apoptosis in hippocampal neurons downstream. Schizophrenia Hippocampal neurons Glycolysis Lactylation HMGB1 Hong, Shijun verfasserin aut Zhang, Xiufeng verfasserin aut Li, Yuwen verfasserin aut Xie, Runfang verfasserin aut Enthalten in Brain research Amsterdam : Elsevier, 1966 1812 Online-Ressource (DE-627)254635776 (DE-600)1462674-3 (DE-576)074530976 1872-6240 nnns volume:1812 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_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 1812
language	English
source	Enthalten in Brain research 1812 volume:1812
sourceStr	Enthalten in Brain research 1812 volume:1812
format_phy_str_mv	Article
bklname	Neurologie
institution	findex.gbv.de
topic_facet	Schizophrenia Hippocampal neurons Glycolysis Lactylation HMGB1
dewey-raw	150
isfreeaccess_bool	false
container_title	Brain research
authorswithroles_txt_mv	Xie, Jiming @@aut@@ Hong, Shijun @@aut@@ Zhang, Xiufeng @@aut@@ Li, Yuwen @@aut@@ Xie, Runfang @@aut@@
publishDateDaySort_date	2023-01-01T00:00:00Z
hierarchy_top_id	254635776
dewey-sort	3150
id	ELV010073647
language_de	englisch
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author	Xie, Jiming
spellingShingle	Xie, Jiming ddc 150 bkl 44.90 misc Schizophrenia misc Hippocampal neurons misc Glycolysis misc Lactylation misc HMGB1 Inhibition of glycolysis prevents behavioural changes in mice with MK801-induced SCZ model by alleviating lactate accumulation and lactylation
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topic_title	150 610 VZ 44.90 bkl Inhibition of glycolysis prevents behavioural changes in mice with MK801-induced SCZ model by alleviating lactate accumulation and lactylation Schizophrenia Hippocampal neurons Glycolysis Lactylation HMGB1
topic	ddc 150 bkl 44.90 misc Schizophrenia misc Hippocampal neurons misc Glycolysis misc Lactylation misc HMGB1
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title	Inhibition of glycolysis prevents behavioural changes in mice with MK801-induced SCZ model by alleviating lactate accumulation and lactylation
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title_full	Inhibition of glycolysis prevents behavioural changes in mice with MK801-induced SCZ model by alleviating lactate accumulation and lactylation
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title_sort	inhibition of glycolysis prevents behavioural changes in mice with mk801-induced scz model by alleviating lactate accumulation and lactylation
title_auth	Inhibition of glycolysis prevents behavioural changes in mice with MK801-induced SCZ model by alleviating lactate accumulation and lactylation
abstract	Schizophrenia (SCZ) is a debilitating neuropsychiatric disorder with a complex aetiology. Cognitive symptoms and hippocampal changes have been implicated in the pathophysiology of SCZ. Changes in metabolites level and up-regulated glycolysis have been reported in previous studies, which may be related to the hippocampal dysfunction in SCZ. However, the pathological mechanism of glycolysis involved in the pathogenesis of SCZ remains unclear. Therefore, the change of glycolysis level and the involvement in SCZ need to be further studied. In our study, MK801 was used to induce an SCZ mouse model and cell model in vivo and in vitro. Western blotting was performed to evaluate the levels of glycolysis, metabolites, and lactylation in hippocampal tissue of mice with SCZ or cell models. The level of high mobility group protein 1 (HMGB1) in the medium of MK801-treated primary hippocampal neurons was examined. Apoptosis was evaluated in HMGB1-treated hippocampal neurons by flow cytometry. The glycolysis inhibitor 2-DG prevented behavioural changes in the MK801-induced SCZ mouse model. The lactate accumulation and level of lactylation were alleviated in the hippocampal tissue of MK801-treated mice. Glycolysis was enhanced, and lactate accumulated in MK-801-treated primary hippocampal neurons. In addition, the level of HMGB1 increased in the medium and induced apoptosis in primary hippocampal neurons. Together, the data showed that glycolysis and lactylation increased in the MK801-induced SCZ model in vivo and in vitro, and this effect could be prevented by 2-DG (a glycolysis inhibitor). Glycolytic related HMGB1 upregulation may induce apoptosis in hippocampal neurons downstream.
abstractGer	Schizophrenia (SCZ) is a debilitating neuropsychiatric disorder with a complex aetiology. Cognitive symptoms and hippocampal changes have been implicated in the pathophysiology of SCZ. Changes in metabolites level and up-regulated glycolysis have been reported in previous studies, which may be related to the hippocampal dysfunction in SCZ. However, the pathological mechanism of glycolysis involved in the pathogenesis of SCZ remains unclear. Therefore, the change of glycolysis level and the involvement in SCZ need to be further studied. In our study, MK801 was used to induce an SCZ mouse model and cell model in vivo and in vitro. Western blotting was performed to evaluate the levels of glycolysis, metabolites, and lactylation in hippocampal tissue of mice with SCZ or cell models. The level of high mobility group protein 1 (HMGB1) in the medium of MK801-treated primary hippocampal neurons was examined. Apoptosis was evaluated in HMGB1-treated hippocampal neurons by flow cytometry. The glycolysis inhibitor 2-DG prevented behavioural changes in the MK801-induced SCZ mouse model. The lactate accumulation and level of lactylation were alleviated in the hippocampal tissue of MK801-treated mice. Glycolysis was enhanced, and lactate accumulated in MK-801-treated primary hippocampal neurons. In addition, the level of HMGB1 increased in the medium and induced apoptosis in primary hippocampal neurons. Together, the data showed that glycolysis and lactylation increased in the MK801-induced SCZ model in vivo and in vitro, and this effect could be prevented by 2-DG (a glycolysis inhibitor). Glycolytic related HMGB1 upregulation may induce apoptosis in hippocampal neurons downstream.
abstract_unstemmed	Schizophrenia (SCZ) is a debilitating neuropsychiatric disorder with a complex aetiology. Cognitive symptoms and hippocampal changes have been implicated in the pathophysiology of SCZ. Changes in metabolites level and up-regulated glycolysis have been reported in previous studies, which may be related to the hippocampal dysfunction in SCZ. However, the pathological mechanism of glycolysis involved in the pathogenesis of SCZ remains unclear. Therefore, the change of glycolysis level and the involvement in SCZ need to be further studied. In our study, MK801 was used to induce an SCZ mouse model and cell model in vivo and in vitro. Western blotting was performed to evaluate the levels of glycolysis, metabolites, and lactylation in hippocampal tissue of mice with SCZ or cell models. The level of high mobility group protein 1 (HMGB1) in the medium of MK801-treated primary hippocampal neurons was examined. Apoptosis was evaluated in HMGB1-treated hippocampal neurons by flow cytometry. The glycolysis inhibitor 2-DG prevented behavioural changes in the MK801-induced SCZ mouse model. The lactate accumulation and level of lactylation were alleviated in the hippocampal tissue of MK801-treated mice. Glycolysis was enhanced, and lactate accumulated in MK-801-treated primary hippocampal neurons. In addition, the level of HMGB1 increased in the medium and induced apoptosis in primary hippocampal neurons. Together, the data showed that glycolysis and lactylation increased in the MK801-induced SCZ model in vivo and in vitro, and this effect could be prevented by 2-DG (a glycolysis inhibitor). Glycolytic related HMGB1 upregulation may induce apoptosis in hippocampal neurons downstream.
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title_short	Inhibition of glycolysis prevents behavioural changes in mice with MK801-induced SCZ model by alleviating lactate accumulation and lactylation
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up_date	2024-07-06T16:43:59.205Z
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Inhibition of glycolysis prevents behavioural changes in mice with MK801-induced SCZ model by alleviating lactate accumulation and lactylation

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