2003 Fiscal Year Final Research Report Summary
Effects of oxidative stress during ischemia-reperfusion on cytokine production in monocytes and lymphocytes
| Project/Area Number |
14370486
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
ARAI Toshiyuki Kyoto University, Medicine, Associated Professor, 医学研究科, 助教授 (80175950)
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| Co-Investigator(Kenkyū-buntansha) |
NAMBA Tsunehisa Kyoto University, Medicine, Assistant Professor, 医学研究科, 助手 (30283609)
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| Project Period (FY) |
2002 – 2003
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| Keywords | monocytes / lymphocytes / T cells / oxidative stress / 6-formylpterin / cell death / immune responses / NF-κB |
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| Research Abstract |
To elucidate the effects of oxidative stress during ischemia-reperfusion on cytokine production in monocytes and lymphocytes, the follwing studies were performed using flow cytometry and biochemical assay.
1) Effects of hydrogen peroxide as an external oxidative stress and 6-formylpterin (6FP) as an internal one on cell death were examined. The results showed that the resistance against an external and an internal oxidative stress were different between monocytes and lymphocytes.
2) Effects of oxidative stress on cytokine production in monocytes were examined. The results showed that neither external nor internal oxidative stress affected the cytokine production in monocytes.
3) Effects of 6FP on cytokine production and cell proliferation in T cells were examined. The results showed that both of the cytokine production and the cell proliferation were suppressed by 6FP.
4) Effects of 6FP on NF-κB activation in T cells were examined. The results showed that 6FP did not affect the translocation of NF-κB but inhibited the NF-κB-dependent transcription.
In conclusion, it was revealed that oxidative stress did not affect the inflammatory responses of monocytes but that oxidative stress suppressed the immune response of T cells by the inhibition of the NF-κB-dependent transcription.
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