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Article: Ginsenoside Rg1 Prevents Chemotherapy-Induced Cognitive Impairment: Associations with Microglia-Mediated Cytokines, Neuroinflammation, and Neuroplasticity

TitleGinsenoside Rg1 Prevents Chemotherapy-Induced Cognitive Impairment: Associations with Microglia-Mediated Cytokines, Neuroinflammation, and Neuroplasticity
Authors
KeywordsGinsenoside Rg1
Chemobrain
Cytokines
Neuroinflammation
Neuroplasticity
Issue Date2019
PublisherSpringer (part of Springer Nature): Springer Open Choice Hybrid Journals. The Journal's web site is located at https://www.springer.com/biomed/neuroscience/journal/12035
Citation
Molecular Neurobiology, 2019, v. 56 n. 8, p. 5626-5642 How to Cite?
AbstractChemotherapy-induced cognitive impairment, also known as “chemobrain,” is a common side effect. The purpose of this study was to examine whether ginsenoside Rg1, a ginseng-derived compound, could prevent chemobrain and its underlying mechanisms. A mouse model of chemobrain was developed with three injections of docetaxel, adriamycin, and cyclophosphamide (DAC) in combination at a 2-day interval. Rg1 (5 and 10 mg/kg daily) was given 1 week prior to DAC regimen for 3 weeks. An amount of 10 mg/kg Rg1 significantly improved chemobrain-like behavior in water maze test. In vivo neuroimaging revealed that Rg1 co-treatment reversed DAC-induced decreases in prefrontal and hippocampal neuronal activity and ameliorated cortical neuronal dendritic spine elimination. It normalized DAC-caused abnormalities in the expression of multiple neuroplasticity biomarkers in the two brain regions. Rg1 suppressed DAC-induced elevation of the proinflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), but increased levels of the anti-inflammatory cytokines IL-4 and IL-10 in multiple sera and brain tissues. Rg1 also modulated cytokine mediators and inhibited DAC-induced microglial polarization from M2 to M1 phenotypes. In in vitro experiments, while impaired viability of PC12 neuroblastic cells and hyperactivation of BV-2 microglial cells, a model of neuroinflammation, were observed in the presence of DAC, Rg1 co-treatment strikingly reduced DAC’s neurotoxic effects and neuroinflammatory response. These results indicate that Rg1 exerts its anti-chemobrain effect in an association with the inhibition of neuroinflammation by modulating microglia-mediated cytokines and the related upstream mediators, protecting neuronal activity and promoting neuroplasticity in particular brain regions associated with cognition processing.
Persistent Identifierhttp://hdl.handle.net/10722/274585
ISSN
2017 Impact Factor: 5.076
2015 SCImago Journal Rankings: 1.819

 

DC FieldValueLanguage
dc.contributor.authorSHI, DD-
dc.contributor.authorHUANG, YH-
dc.contributor.authorLai, CSW-
dc.contributor.authorDONG, CM-
dc.contributor.authorHo, LC-
dc.contributor.authorLI, XY-
dc.contributor.authorWu, EX-
dc.contributor.authorLi, Q-
dc.contributor.authorWang, XM-
dc.contributor.authorChen, YJ-
dc.contributor.authorChung, SK-
dc.contributor.authorZhang, ZJ-
dc.date.accessioned2019-08-18T15:04:43Z-
dc.date.available2019-08-18T15:04:43Z-
dc.date.issued2019-
dc.identifier.citationMolecular Neurobiology, 2019, v. 56 n. 8, p. 5626-5642-
dc.identifier.issn0893-7648-
dc.identifier.urihttp://hdl.handle.net/10722/274585-
dc.description.abstractChemotherapy-induced cognitive impairment, also known as “chemobrain,” is a common side effect. The purpose of this study was to examine whether ginsenoside Rg1, a ginseng-derived compound, could prevent chemobrain and its underlying mechanisms. A mouse model of chemobrain was developed with three injections of docetaxel, adriamycin, and cyclophosphamide (DAC) in combination at a 2-day interval. Rg1 (5 and 10 mg/kg daily) was given 1 week prior to DAC regimen for 3 weeks. An amount of 10 mg/kg Rg1 significantly improved chemobrain-like behavior in water maze test. In vivo neuroimaging revealed that Rg1 co-treatment reversed DAC-induced decreases in prefrontal and hippocampal neuronal activity and ameliorated cortical neuronal dendritic spine elimination. It normalized DAC-caused abnormalities in the expression of multiple neuroplasticity biomarkers in the two brain regions. Rg1 suppressed DAC-induced elevation of the proinflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), but increased levels of the anti-inflammatory cytokines IL-4 and IL-10 in multiple sera and brain tissues. Rg1 also modulated cytokine mediators and inhibited DAC-induced microglial polarization from M2 to M1 phenotypes. In in vitro experiments, while impaired viability of PC12 neuroblastic cells and hyperactivation of BV-2 microglial cells, a model of neuroinflammation, were observed in the presence of DAC, Rg1 co-treatment strikingly reduced DAC’s neurotoxic effects and neuroinflammatory response. These results indicate that Rg1 exerts its anti-chemobrain effect in an association with the inhibition of neuroinflammation by modulating microglia-mediated cytokines and the related upstream mediators, protecting neuronal activity and promoting neuroplasticity in particular brain regions associated with cognition processing.-
dc.languageeng-
dc.publisherSpringer (part of Springer Nature): Springer Open Choice Hybrid Journals. The Journal's web site is located at https://www.springer.com/biomed/neuroscience/journal/12035-
dc.relation.ispartofMolecular Neurobiology-
dc.subjectGinsenoside Rg1-
dc.subjectChemobrain-
dc.subjectCytokines-
dc.subjectNeuroinflammation-
dc.subjectNeuroplasticity-
dc.titleGinsenoside Rg1 Prevents Chemotherapy-Induced Cognitive Impairment: Associations with Microglia-Mediated Cytokines, Neuroinflammation, and Neuroplasticity-
dc.typeArticle-
dc.identifier.emailLai, CSW: coraswl@hku.hk-
dc.identifier.emailWu, EX: ewu@eee.hku.hk-
dc.identifier.emailLi, Q: liqi@hkucc.hku.hk-
dc.identifier.emailWang, XM: xmwang1@hku.hk-
dc.identifier.emailChung, SK: skchung@hkucc.hku.hk-
dc.identifier.emailZhang, ZJ: zhangzj@hkucc.hku.hk-
dc.identifier.authorityLai, CSW=rp01895-
dc.identifier.authorityWu, EX=rp00193-
dc.identifier.authorityChung, SK=rp00381-
dc.identifier.authorityZhang, ZJ=rp01297-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s12035-019-1474-9-
dc.identifier.pmid30659419-
dc.identifier.scopuseid_2-s2.0-85060334204-
dc.identifier.hkuros302160-
dc.identifier.volume56-
dc.identifier.issue8-
dc.identifier.spage5626-
dc.identifier.epage5642-
dc.publisher.placeUnited States-

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