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Article: Ceftriaxone ameliorates motor deficits and protects dopaminergic neurons in 6-hydroxydopamine-lesioned rats

TitleCeftriaxone ameliorates motor deficits and protects dopaminergic neurons in 6-hydroxydopamine-lesioned rats
Authors
KeywordsAnimal model of parkinson's disease
Antibiotic
Ceftriaxone
Degeneration of dopaminergic neurons
Glutamate transporter
Issue Date2012
PublisherAmerican Chemical Society.
Citation
ACS Chemical Neuroscience , 2012, v. 3 n. 1, p. 22-30 How to Cite?
AbstractParkinson's disease is caused by the degeneration of dopaminergic neurons in substantia nigra. There is no current promising treatment for neuroprotection of dopaminergic neurons. Ceftriaxone is a beta-lactam antibiotic and has been reported to offer neuroprotective effects (Rothstein, J.-D., Patel, S., Regan, M.-R., Haenggeli, C., Huang, Y.-H., Bergles, D.-E., Jin, L., Dykes, H.-M., Vidensky, S., Chung, D.-S., Toan, S.-V., Bruijn, L.-I., Su, Z.-Z., Gupta, P., and Fisher, P.-B. (2005) Beta-lactam antibiotics offer neuroprotection by increasing glutamate transporter expression Nature433, 73-77). In the present study, efficacy of ceftriaxone in neuroprotection of dopaminergic neurons and amelioration of motor deficits in a rat model of Parkinson's disease were investigated. Ceftriaxone was administrated in 6-hydroxydopamine-lesioned rats. Using behavioral tests, grip strength and numbers of apomorphine-induced contralateral rotation were declined in the ceftriaxone-treated group. More importantly, cell death of dopaminergic neurons was found to decrease. In addition, both the protein expression and immunoreactivity for GLT-1 were up-regulated. The present results strongly indicate that ceftriaxone is a potential agent in the treatment of Parkinson's disease.
Persistent Identifierhttp://hdl.handle.net/10722/164524
ISSN
2015 Impact Factor: 4.348
2015 SCImago Journal Rankings: 1.842
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLeung, TCHen_US
dc.contributor.authorLui, CNPen_US
dc.contributor.authorChen, LWen_US
dc.contributor.authorYung, WHen_US
dc.contributor.authorChan, YSen_US
dc.contributor.authorYung, KKLen_US
dc.date.accessioned2012-09-20T08:05:18Z-
dc.date.available2012-09-20T08:05:18Z-
dc.date.issued2012en_US
dc.identifier.citationACS Chemical Neuroscience , 2012, v. 3 n. 1, p. 22-30en_US
dc.identifier.issn1948-7193-
dc.identifier.urihttp://hdl.handle.net/10722/164524-
dc.description.abstractParkinson's disease is caused by the degeneration of dopaminergic neurons in substantia nigra. There is no current promising treatment for neuroprotection of dopaminergic neurons. Ceftriaxone is a beta-lactam antibiotic and has been reported to offer neuroprotective effects (Rothstein, J.-D., Patel, S., Regan, M.-R., Haenggeli, C., Huang, Y.-H., Bergles, D.-E., Jin, L., Dykes, H.-M., Vidensky, S., Chung, D.-S., Toan, S.-V., Bruijn, L.-I., Su, Z.-Z., Gupta, P., and Fisher, P.-B. (2005) Beta-lactam antibiotics offer neuroprotection by increasing glutamate transporter expression Nature433, 73-77). In the present study, efficacy of ceftriaxone in neuroprotection of dopaminergic neurons and amelioration of motor deficits in a rat model of Parkinson's disease were investigated. Ceftriaxone was administrated in 6-hydroxydopamine-lesioned rats. Using behavioral tests, grip strength and numbers of apomorphine-induced contralateral rotation were declined in the ceftriaxone-treated group. More importantly, cell death of dopaminergic neurons was found to decrease. In addition, both the protein expression and immunoreactivity for GLT-1 were up-regulated. The present results strongly indicate that ceftriaxone is a potential agent in the treatment of Parkinson's disease.-
dc.languageengen_US
dc.publisherAmerican Chemical Society.-
dc.relation.ispartofACS Chemical Neuroscienceen_US
dc.subjectAnimal model of parkinson's disease-
dc.subjectAntibiotic-
dc.subjectCeftriaxone-
dc.subjectDegeneration of dopaminergic neurons-
dc.subjectGlutamate transporter-
dc.titleCeftriaxone ameliorates motor deficits and protects dopaminergic neurons in 6-hydroxydopamine-lesioned ratsen_US
dc.typeArticleen_US
dc.identifier.emailChan, YS: yschan@hku.hken_US
dc.identifier.authorityChan, YS=rp00318en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1021/cn200072h-
dc.identifier.pmid22860178-
dc.identifier.pmcidPMC3369786-
dc.identifier.scopuseid_2-s2.0-84862930096-
dc.identifier.hkuros209196en_US
dc.identifier.volume3en_US
dc.identifier.issue1-
dc.identifier.spage22en_US
dc.identifier.epage30en_US
dc.identifier.isiWOS:000299353800005-
dc.publisher.placeUnited States-

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