Olanzapine Ameliorates Ischemic Stroke-like Pathology in Gerbils and H<sub<2</sub<O<sub<2</sub<-Induced Neurotoxicity in SH-SY5Y Cells via Inhibiting the MAPK Signaling Pathway

Olanzapine (OLNZ) is used to treat psychotic disorders. To look into the neurological basis of this phenomenon, we investigated the neuroprotective effects of OLNZ in gerbils and SH-SY5Y cells. Gerbils were subjected to transient global cerebral ischemia (TGCI) by blocking both common carotid arteri...
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Autor*in:	Md Sadikul Islam [verfasserIn] Ha-Young Shin [verfasserIn] Yeo-Jin Yoo [verfasserIn] Ryunhee Kim [verfasserIn] Young-Jin Jang [verfasserIn] Md Rashedunnabi Akanda [verfasserIn] Hyun-Jin Tae [verfasserIn] In-Shik Kim [verfasserIn] Dongchoon Ahn [verfasserIn] Byung-Yong Park [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	olanzapine transient ischemia oxidative stress neuroprotection antioxidant MAPK

Übergeordnetes Werk:	In: Antioxidants - MDPI AG, 2013, 11(2022), 9, p 1697
Übergeordnetes Werk:	volume:11 ; year:2022 ; number:9, p 1697

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3390/antiox11091697

Katalog-ID:	DOAJ023357177

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allfieldsSound	10.3390/antiox11091697 doi (DE-627)DOAJ023357177 (DE-599)DOAJ6989f713ec2b49a8b93081c52ea47986 DE-627 ger DE-627 rakwb eng RM1-950 Md Sadikul Islam verfasserin aut Olanzapine Ameliorates Ischemic Stroke-like Pathology in Gerbils and H<sub<2</sub<O<sub<2</sub<-Induced Neurotoxicity in SH-SY5Y Cells via Inhibiting the MAPK Signaling Pathway 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Olanzapine (OLNZ) is used to treat psychotic disorders. To look into the neurological basis of this phenomenon, we investigated the neuroprotective effects of OLNZ in gerbils and SH-SY5Y cells. Gerbils were subjected to transient global cerebral ischemia (TGCI) by blocking both common carotid arteries, and OLNZ (10 mg/kg) was injected intraperitoneally. Hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) was used to induce oxidative-stress-mediated damage in the SH-SY5Y cells. The results indicated that OLNZ administration markedly reduced neuron damage and glial cell triggering within CA1 zone of the hippocampus. We used RNA sequencing to assess the numbers of up-and downregulated genes involved in TGCI. We found that OLNZ treatment downregulated the expression of complement-component-related genes and the expression of mitogen-activated protein kinases (MAPKs) in the hippocampus. In cells, OLNZ co-treatment significantly improved cell viability and reduced lactate dehydrogenase (LDH), and reactive oxygen species (ROS) generation. Expression of antioxidant superoxide dismutase-1,2 enzymes (SOD-1, SOD-2) was also intensely upregulated by OLNZ, while the expression of MAPKs and NF-κB were reduced. Co-incubation with OLNZ also regulated apoptosis-related proteins Bax/Bcl-2 expression. Finally, the results demonstrated that treatment with OLNZ showed neuroprotective effects and that the MAPK pathway could involve in the protective effects. olanzapine transient ischemia oxidative stress neuroprotection antioxidant MAPK Therapeutics. Pharmacology Ha-Young Shin verfasserin aut Yeo-Jin Yoo verfasserin aut Ryunhee Kim verfasserin aut Young-Jin Jang verfasserin aut Md Rashedunnabi Akanda verfasserin aut Hyun-Jin Tae verfasserin aut In-Shik Kim verfasserin aut Dongchoon Ahn verfasserin aut Byung-Yong Park verfasserin aut In Antioxidants MDPI AG, 2013 11(2022), 9, p 1697 (DE-627)737287578 (DE-600)2704216-9 20763921 nnns volume:11 year:2022 number:9, p 1697 https://doi.org/10.3390/antiox11091697 kostenfrei https://doaj.org/article/6989f713ec2b49a8b93081c52ea47986 kostenfrei https://www.mdpi.com/2076-3921/11/9/1697 kostenfrei https://doaj.org/toc/2076-3921 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2022 9, p 1697
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authorswithroles_txt_mv	Md Sadikul Islam @@aut@@ Ha-Young Shin @@aut@@ Yeo-Jin Yoo @@aut@@ Ryunhee Kim @@aut@@ Young-Jin Jang @@aut@@ Md Rashedunnabi Akanda @@aut@@ Hyun-Jin Tae @@aut@@ In-Shik Kim @@aut@@ Dongchoon Ahn @@aut@@ Byung-Yong Park @@aut@@
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callnumber-first	R - Medicine
author	Md Sadikul Islam
spellingShingle	Md Sadikul Islam misc RM1-950 misc olanzapine misc transient ischemia misc oxidative stress misc neuroprotection misc antioxidant misc MAPK misc Therapeutics. Pharmacology Olanzapine Ameliorates Ischemic Stroke-like Pathology in Gerbils and H<sub<2</sub<O<sub<2</sub<-Induced Neurotoxicity in SH-SY5Y Cells via Inhibiting the MAPK Signaling Pathway
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topic_title	RM1-950 Olanzapine Ameliorates Ischemic Stroke-like Pathology in Gerbils and H<sub<2</sub<O<sub<2</sub<-Induced Neurotoxicity in SH-SY5Y Cells via Inhibiting the MAPK Signaling Pathway olanzapine transient ischemia oxidative stress neuroprotection antioxidant MAPK
topic	misc RM1-950 misc olanzapine misc transient ischemia misc oxidative stress misc neuroprotection misc antioxidant misc MAPK misc Therapeutics. Pharmacology
topic_unstemmed	misc RM1-950 misc olanzapine misc transient ischemia misc oxidative stress misc neuroprotection misc antioxidant misc MAPK misc Therapeutics. Pharmacology
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title	Olanzapine Ameliorates Ischemic Stroke-like Pathology in Gerbils and H<sub<2</sub<O<sub<2</sub<-Induced Neurotoxicity in SH-SY5Y Cells via Inhibiting the MAPK Signaling Pathway
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title_full	Olanzapine Ameliorates Ischemic Stroke-like Pathology in Gerbils and H<sub<2</sub<O<sub<2</sub<-Induced Neurotoxicity in SH-SY5Y Cells via Inhibiting the MAPK Signaling Pathway
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title_sort	olanzapine ameliorates ischemic stroke-like pathology in gerbils and h<sub<2</sub<o<sub<2</sub<-induced neurotoxicity in sh-sy5y cells via inhibiting the mapk signaling pathway
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title_auth	Olanzapine Ameliorates Ischemic Stroke-like Pathology in Gerbils and H<sub<2</sub<O<sub<2</sub<-Induced Neurotoxicity in SH-SY5Y Cells via Inhibiting the MAPK Signaling Pathway
abstract	Olanzapine (OLNZ) is used to treat psychotic disorders. To look into the neurological basis of this phenomenon, we investigated the neuroprotective effects of OLNZ in gerbils and SH-SY5Y cells. Gerbils were subjected to transient global cerebral ischemia (TGCI) by blocking both common carotid arteries, and OLNZ (10 mg/kg) was injected intraperitoneally. Hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) was used to induce oxidative-stress-mediated damage in the SH-SY5Y cells. The results indicated that OLNZ administration markedly reduced neuron damage and glial cell triggering within CA1 zone of the hippocampus. We used RNA sequencing to assess the numbers of up-and downregulated genes involved in TGCI. We found that OLNZ treatment downregulated the expression of complement-component-related genes and the expression of mitogen-activated protein kinases (MAPKs) in the hippocampus. In cells, OLNZ co-treatment significantly improved cell viability and reduced lactate dehydrogenase (LDH), and reactive oxygen species (ROS) generation. Expression of antioxidant superoxide dismutase-1,2 enzymes (SOD-1, SOD-2) was also intensely upregulated by OLNZ, while the expression of MAPKs and NF-κB were reduced. Co-incubation with OLNZ also regulated apoptosis-related proteins Bax/Bcl-2 expression. Finally, the results demonstrated that treatment with OLNZ showed neuroprotective effects and that the MAPK pathway could involve in the protective effects.
abstractGer	Olanzapine (OLNZ) is used to treat psychotic disorders. To look into the neurological basis of this phenomenon, we investigated the neuroprotective effects of OLNZ in gerbils and SH-SY5Y cells. Gerbils were subjected to transient global cerebral ischemia (TGCI) by blocking both common carotid arteries, and OLNZ (10 mg/kg) was injected intraperitoneally. Hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) was used to induce oxidative-stress-mediated damage in the SH-SY5Y cells. The results indicated that OLNZ administration markedly reduced neuron damage and glial cell triggering within CA1 zone of the hippocampus. We used RNA sequencing to assess the numbers of up-and downregulated genes involved in TGCI. We found that OLNZ treatment downregulated the expression of complement-component-related genes and the expression of mitogen-activated protein kinases (MAPKs) in the hippocampus. In cells, OLNZ co-treatment significantly improved cell viability and reduced lactate dehydrogenase (LDH), and reactive oxygen species (ROS) generation. Expression of antioxidant superoxide dismutase-1,2 enzymes (SOD-1, SOD-2) was also intensely upregulated by OLNZ, while the expression of MAPKs and NF-κB were reduced. Co-incubation with OLNZ also regulated apoptosis-related proteins Bax/Bcl-2 expression. Finally, the results demonstrated that treatment with OLNZ showed neuroprotective effects and that the MAPK pathway could involve in the protective effects.
abstract_unstemmed	Olanzapine (OLNZ) is used to treat psychotic disorders. To look into the neurological basis of this phenomenon, we investigated the neuroprotective effects of OLNZ in gerbils and SH-SY5Y cells. Gerbils were subjected to transient global cerebral ischemia (TGCI) by blocking both common carotid arteries, and OLNZ (10 mg/kg) was injected intraperitoneally. Hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) was used to induce oxidative-stress-mediated damage in the SH-SY5Y cells. The results indicated that OLNZ administration markedly reduced neuron damage and glial cell triggering within CA1 zone of the hippocampus. We used RNA sequencing to assess the numbers of up-and downregulated genes involved in TGCI. We found that OLNZ treatment downregulated the expression of complement-component-related genes and the expression of mitogen-activated protein kinases (MAPKs) in the hippocampus. In cells, OLNZ co-treatment significantly improved cell viability and reduced lactate dehydrogenase (LDH), and reactive oxygen species (ROS) generation. Expression of antioxidant superoxide dismutase-1,2 enzymes (SOD-1, SOD-2) was also intensely upregulated by OLNZ, while the expression of MAPKs and NF-κB were reduced. Co-incubation with OLNZ also regulated apoptosis-related proteins Bax/Bcl-2 expression. Finally, the results demonstrated that treatment with OLNZ showed neuroprotective effects and that the MAPK pathway could involve in the protective effects.
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container_issue	9, p 1697
title_short	Olanzapine Ameliorates Ischemic Stroke-like Pathology in Gerbils and H<sub<2</sub<O<sub<2</sub<-Induced Neurotoxicity in SH-SY5Y Cells via Inhibiting the MAPK Signaling Pathway
url	https://doi.org/10.3390/antiox11091697 https://doaj.org/article/6989f713ec2b49a8b93081c52ea47986 https://www.mdpi.com/2076-3921/11/9/1697 https://doaj.org/toc/2076-3921
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To look into the neurological basis of this phenomenon, we investigated the neuroprotective effects of OLNZ in gerbils and SH-SY5Y cells. Gerbils were subjected to transient global cerebral ischemia (TGCI) by blocking both common carotid arteries, and OLNZ (10 mg/kg) was injected intraperitoneally. Hydrogen peroxide (H<sub<2</sub<O<sub<2</sub<) was used to induce oxidative-stress-mediated damage in the SH-SY5Y cells. The results indicated that OLNZ administration markedly reduced neuron damage and glial cell triggering within CA1 zone of the hippocampus. We used RNA sequencing to assess the numbers of up-and downregulated genes involved in TGCI. We found that OLNZ treatment downregulated the expression of complement-component-related genes and the expression of mitogen-activated protein kinases (MAPKs) in the hippocampus. In cells, OLNZ co-treatment significantly improved cell viability and reduced lactate dehydrogenase (LDH), and reactive oxygen species (ROS) generation. Expression of antioxidant superoxide dismutase-1,2 enzymes (SOD-1, SOD-2) was also intensely upregulated by OLNZ, while the expression of MAPKs and NF-κB were reduced. Co-incubation with OLNZ also regulated apoptosis-related proteins Bax/Bcl-2 expression. 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Olanzapine Ameliorates Ischemic Stroke-like Pathology in Gerbils and H<sub<2</sub<O<sub<2</sub<-Induced Neurotoxicity in SH-SY5Y Cells via Inhibiting the MAPK Signaling Pathway

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