2022 Fiscal Year Annual Research Report
Does the combination of nicotine and ethanol facilitate or block dopaminergic neuron damage in Parkinson's disease models?
Project/Area Number |
19K10687
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Research Institution | Kagawa University |
Principal Investigator |
モストファ ジャーマル 香川大学, 医学部, 助教 (50418802)
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Co-Investigator(Kenkyū-buntansha) |
塚本 郁子 香川大学, 医学部, 寄附講座教員 (10183477)
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Project Period (FY) |
2019-04-01 – 2023-03-31
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Keywords | ethanol / nicotine / Dopamine / tyrosine hydroxylase / MPTP-treated mice |
Outline of Annual Research Achievements |
EtOH (2.0 and 3.0 g/kg) alone reversed the effects of MPTP treatment in the striatum and hippocampus, as evidenced by an increase in DA, DOPAC, and HVA levels, TH expression, and Ser31 phosphorylation compared to the control. Likewise, NIC (1.0 and 2.0 mg/kg) alone reversed MPTP treatment effects, with treated mice showing increased DA, DOPAC, and HVA contents, TH expression, and Ser31 phosphorylation compared to control mice. Co-administration of EtOH (2.0 g/kg) and NIC (1.0 mg/kg) further increased DA and HVA tissue contents, TH expression, and Ser31 phosphorylation, indicating an additive effect. These results show EtOH and NIC showed an additive effect in combination, suggesting that their co-application could be a potent therapeutic strategy for treating PD.
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