Clarification of the mechanism of cutaneous inflammation by analyzing the change of redox balance
| Project/Area Number |
15591198
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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 |
Dermatology
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| Research Institution | Nippon Medical School |
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Principal Investigator |
YAMAOKA Junichi Nippon Medical School, Department of Dermatology, Lecturer, 医学部, 講師 (80283688)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2004: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2003: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | redox balance / oxidative stress / nitric oxide(NO) / apoptosis / cutaneous inflammation / ultraviolet B(UVB) / mouse model / NO / UVB / 虚血再灌流 / モデルマウス / 血管障害 |
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| Research Abstract |
In the pathogenesis of various cutaneous inflammations, redox balance (balance between oxidative stress and anti-oxidants or anti-oxidative enzymes) is playing essentially important roles. In this research, I tried to clarify the redox balance in the cutaneous inflammation. I focused the research subjects on the following two points.
1,Suppression of ultraviolet B(UVB)-induced keratinocyte apoptosis by moderate doses of nitric oxide(NO).
It is well known that UVB induces keratinocyte apoptosis, in which oxidative stress seems to be involved. I examined the effect of NO on this response. As a result, I found that moderate doses of NO suppress UVB-induced keratinocyte apoptosis. In addition, Moderate doses of NO suppress several molecules in the apoptotic signaling cascades such as p53, caspase 8, caspase 9 and caspase 3, and that NO activates Bcl-2. Through these mechanisms, NO might inhibit UVB-induced keratinocyte apoptosis. However, the reason why NO has this effect is not clear now. It may possibly happen through the reaction of NO to the other redox modulating agents.
2,Development of model mice for the analyses of redox balance in the cutaneous inflammation.
As models which may develop cutaneous inflammation, I made up several model mice for (1)skin ischemia by oppression, (2)skin wound, (3)ultraviolet radiation on the skin, (4)skin scratching. At present, I have just started analyses about redox balance in these model mice. Further analyses will be done to clarify the role of redox balance in the cutaneous inflammation by using these model mice.
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Report
(3 results)
Research Products
(4 results)
