title: The antioxidant drink effective microorganism-X (EM-X) pre-treatment attenuates the loss of nigrostriatal dopaminergic neurons in 6-hydroxydopamine-lesion rat model of Parkinson's disease.
abstract: There is continued interest in the assessment and potential use of antioxidants as neuroprotective agents in diseases associated with increased oxidative stress, such as Parkinson's disease. The neuroprotective effect of a natural antioxidant drink, EM-X (a ferment derivative of unpolished rice, papaya and seaweeds with effective microorganisms), was investigated using the 6-hydroxydopamine (6-OHDA)-lesion rat model of Parkinson's disease. The nigrostriatal dopaminergic neurons were unilaterally lesioned with 6-OHDA (8 microg) in rats that were treated with a 10-times diluted EM-X drink (dilEM-X), standard EM-X drink (stdEM-X) or tap water for 4 days. Seven days post lesion, the integrity (no. of tyrosine hydroxylase positive cells (TH+ cells) in the substantia nigra pars compacta (SNpc)) and functionality (dopamine and its metabolites DOPAC and HVA content in the striata) of nigrostriatal dopaminergic neurons were assessed. In the vehicle-treated rats, infusion of 8 microg of 6-OHDA significantly reduced the number of TH+ cells in the SNpc as well as the levels of dopamine, DOPAC and HVA in the striata on the lesion side. The loss of TH+ cells, dopamine and HVA, but not the DOPAC levels, was significantly attenuated by stdEM-X pretreatment, but not by the dilEM-X pretreatment. There were no significant changes in the TH+ cells, or in the monoamine levels with the EM-X pretreatment per se, except for a small but significant fall in the levels of dopamine with the stdEM-X. The evidence presented supports the potential neuroprotective effects of stdEM-X drink, although its effect on dopamine levels needs further investigation.
authors.affiliation: Department of Neuroinflammation, Faculty of Medicine, Imperial College London, Charing Cross Hospital Campus, Fulham Palace Road, London W6 8RF, UK.
authors.forename: K P
authors.initials: KP
authors.lastname: Datla
authors.forename: R D
authors.initials: RD
authors.lastname: Bennett
authors.forename: V
authors.initials: V
authors.lastname: Zbarsky
authors.forename: B
authors.initials: B
authors.lastname: Ke
authors.forename: Y-F
authors.initials: YF
authors.lastname: Liang
authors.forename: T
authors.initials: T
authors.lastname: Higa
authors.forename: T
authors.initials: T
authors.lastname: Bahorun
authors.forename: O I
authors.initials: OI
authors.lastname: Aruoma
authors.forename: D T
authors.initials: DT
authors.lastname: Dexter
mesh_terms: D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000494:pharmacology*; D001628:Beverages; D003342:Corpus Striatum / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D004298:Dopamine / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D006027:Glycosides / Q000494:pharmacology*; D044949:Kaempferols / Q000494:pharmacology*; D008297:Male; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism; D018696:Neuroprotective Agents / Q000008:administration & dosage / Q000494:pharmacology*; D016627:Oxidopamine; D010300:Parkinson Disease / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013378:Substantia Nigra / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D013997:Time Factors; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D006027:Glycosides; D044949:Kaempferols; D018696:Neuroprotective Agents; C087919:kaempferol-3-O-glucopyranosyl-1-4-rhamnopyranoside; D015102:3,4-Dihydroxyphenylacetic Acid; D016627:Oxidopamine; D014446:Tyrosine 3-Monooxygenase; D004298:Dopamine