| Project/Area Number |
18580123
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Food science
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| Research Institution | Kyushu University |
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Principal Investigator |
TERUYA Kiichiro Kyushu University, Faculty of Agriculture, Assistant Professor (10273971)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,890,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥390,000)
Fiscal Year 2007: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2006: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | cell, tissue / foods / cranial nerve disorders / stress / signal transduction |
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| Research Abstract |
Fermented milk Kefir, enzyme-digested fucoidan extracts and electrorized reduced water were investigated as anti-Parkinson's disease functions. To evaluate suppression of cytotoxicity induced nitric oxide (NO) donor, human dopaminergic neuron model SH-SY5Y cells were treated with SIN-1 or sodium nitroprusside. The cytotoxicity was determined by WST-1 assay. An apoptosis was evaluated by immunoblotting about caspase activations. However, candidate functional foods and waters were not effective for protection of dopaminergic neurons against NO donor.
To evaluate activation for protein quality control system in SH-SY5Y cells were treated with potent proteasome inhibitor MG-132. The treatment of enzyme-digested fucoidan extracts suppressed the ubiquitinated protein accumulation in the cells, and increased the proteasome activities.
The enzyme-digested fucoidan extracts were orally administrated Parkinson's disease model mouse (MPTP and probenecid administrated C57BL/6J male mice). It was observed that depression of spontaneous movement was suppressed and tyrosine hydroxylase expression in mid brain was protected against MPTP damages. Since, tyrosine hydroxylase is the key enzyme of dopamine synthesis, it was suggested that the enzyme-digested fucoidan extract had the protective effect for dopaminergic neurons against MPTP damages.
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