PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31679397-1	2020	Aim: The aim of this study is to investigate whether lithium chloride (LiCl) can regulate glycogen synthase kinase-3beta (GSK3beta)/nuclear factor E2 related factor(Nrf2)/heme oxygenase-1 (HO-1) pathway to reduce the injury of oxidative stress in APP/PS1 double transgenic mice.Materials and Methods: The APP/PS1 double transgenic and wild-type (WT) mice were divided randomly into four groups, i.e. WT, WT + LiCl (LiCl 100 mg/kg by gavage once daily), the transgenic + LiCl and the transgenic groups.	Lithium Chloride	409-413	nuclear factor, erythroid derived 2, like 2	Mus musculus	165-169	
31679397-0	2020	Lithium chloride reduced the level of oxidative stress in brains and serums of APP/PS1 double transgenic mice via the regulation of GSK3beta/Nrf2/HO-1 pathway.	Lithium Chloride	0-16	nuclear factor, erythroid derived 2, like 2	Mus musculus	141-145	
31679397-1	2020	Aim: The aim of this study is to investigate whether lithium chloride (LiCl) can regulate glycogen synthase kinase-3beta (GSK3beta)/nuclear factor E2 related factor(Nrf2)/heme oxygenase-1 (HO-1) pathway to reduce the injury of oxidative stress in APP/PS1 double transgenic mice.Materials and Methods: The APP/PS1 double transgenic and wild-type (WT) mice were divided randomly into four groups, i.e. WT, WT + LiCl (LiCl 100 mg/kg by gavage once daily), the transgenic + LiCl and the transgenic groups.	Lithium Chloride	53-69	nuclear factor, erythroid derived 2, like 2	Mus musculus	165-169	
31679397-1	2020	Aim: The aim of this study is to investigate whether lithium chloride (LiCl) can regulate glycogen synthase kinase-3beta (GSK3beta)/nuclear factor E2 related factor(Nrf2)/heme oxygenase-1 (HO-1) pathway to reduce the injury of oxidative stress in APP/PS1 double transgenic mice.Materials and Methods: The APP/PS1 double transgenic and wild-type (WT) mice were divided randomly into four groups, i.e. WT, WT + LiCl (LiCl 100 mg/kg by gavage once daily), the transgenic + LiCl and the transgenic groups.	Lithium Chloride	71-75	nuclear factor, erythroid derived 2, like 2	Mus musculus	165-169	
31679397-1	2020	Aim: The aim of this study is to investigate whether lithium chloride (LiCl) can regulate glycogen synthase kinase-3beta (GSK3beta)/nuclear factor E2 related factor(Nrf2)/heme oxygenase-1 (HO-1) pathway to reduce the injury of oxidative stress in APP/PS1 double transgenic mice.Materials and Methods: The APP/PS1 double transgenic and wild-type (WT) mice were divided randomly into four groups, i.e. WT, WT + LiCl (LiCl 100 mg/kg by gavage once daily), the transgenic + LiCl and the transgenic groups.	Lithium Chloride	409-413	nuclear factor, erythroid derived 2, like 2	Mus musculus	165-169	
31679397-1	2020	Aim: The aim of this study is to investigate whether lithium chloride (LiCl) can regulate glycogen synthase kinase-3beta (GSK3beta)/nuclear factor E2 related factor(Nrf2)/heme oxygenase-1 (HO-1) pathway to reduce the injury of oxidative stress in APP/PS1 double transgenic mice.Materials and Methods: The APP/PS1 double transgenic and wild-type (WT) mice were divided randomly into four groups, i.e. WT, WT + LiCl (LiCl 100 mg/kg by gavage once daily), the transgenic + LiCl and the transgenic groups.	Lithium Chloride	409-413	nuclear factor, erythroid derived 2, like 2	Mus musculus	165-169	
31679397-5	2020	The treatment with LiCl attenuated these changes in the levels of GSK3beta/Nrf2/HO-1 pathway and oxidative stress as well as Nissl bodies induced by APP/PS1 mutation.Conclusion: LiCl reversed the declined activities of SOD and GSH-Px and the increased content of MDA as well as the decreased Nissl bodies in neurons in the brains or serums of APP/PS1 mice, the mechanism of which may be involved in the down-regulation of the activity of GSK3beta and consequently enhances the expressions of Nrf2 and HO-1.	Lithium Chloride	19-23	nuclear factor, erythroid derived 2, like 2	Mus musculus	75-79	
31679397-5	2020	The treatment with LiCl attenuated these changes in the levels of GSK3beta/Nrf2/HO-1 pathway and oxidative stress as well as Nissl bodies induced by APP/PS1 mutation.Conclusion: LiCl reversed the declined activities of SOD and GSH-Px and the increased content of MDA as well as the decreased Nissl bodies in neurons in the brains or serums of APP/PS1 mice, the mechanism of which may be involved in the down-regulation of the activity of GSK3beta and consequently enhances the expressions of Nrf2 and HO-1.	Lithium Chloride	19-23	nuclear factor, erythroid derived 2, like 2	Mus musculus	492-496	
31679397-5	2020	The treatment with LiCl attenuated these changes in the levels of GSK3beta/Nrf2/HO-1 pathway and oxidative stress as well as Nissl bodies induced by APP/PS1 mutation.Conclusion: LiCl reversed the declined activities of SOD and GSH-Px and the increased content of MDA as well as the decreased Nissl bodies in neurons in the brains or serums of APP/PS1 mice, the mechanism of which may be involved in the down-regulation of the activity of GSK3beta and consequently enhances the expressions of Nrf2 and HO-1.	Lithium Chloride	178-182	nuclear factor, erythroid derived 2, like 2	Mus musculus	492-496	
29659176-4	2018	Here we showed that treatment with a Wnt pathway activator (LiCl) reduced elastase-induced airspace enlargement and cigarette smoke extract (CSE)-induced lung inflammatory responses in WT mice, which was associated with increased activation of Nrf2 pathway.	Lithium Chloride	60-64	nuclear factor, erythroid derived 2, like 2	Mus musculus	244-248