| Project/Area Number |
11671507
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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 |
Anesthesiology/Resuscitation studies
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| Research Institution | NAGASAKI UNIVERSITY |
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Principal Investigator |
MOROOKA Hiroaki University Hospital, NAGASAKI UNIVERSITY, Associate Professor, 医学部, 助教授 (70230175)
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| Co-Investigator(Kenkyū-buntansha) |
TUJITA Toshiya University Hospital, NAGASAKI UNIVERSITY, Instructor, 医学部・附属病院, 助手 (40244066)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2001: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2000: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1999: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | SAPK / LNK / p38 MAPK / Ischemia-Reperfusion / p38MAPK / p38 MAP キナーゼ / 高体温 |
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| Research Abstract |
p38 mitogen-activated protein kinase (MAPK) plays an important role in regulating gene expression. p38 MAPK as well as stress-activated protein kinase (SAPK/JNK) is activated in response to a variety of cellular stresses, such as heat stress and oxidative stress. N-acetyl-L-cysteine ' (NAC), an antioxidant, increases the intracellular glutathione (GSH) levels and attenuates SAPK/JNK activity resulting in reduced cellular damage. We investigated the effect of NAC on the activatiomofp38 MAPK in heat stressed rat heart. 12 male Wistar rats were anesthetized with pentobarbital intraperitoneally (i.p.). Saline (n=6) or 1 mmol/kg NAC (n=6) were administered i.p. 60 min before treatment withbody temperature. Desired bodytemperature (37 or 41 C) was achieved by placing animals in a positive forced air incubator. Heart was removed 60 min follwing the samebodytemperature. p38 MAPK activity at 41 Cwas increased to 630±53 % of that at 37 C. NAC administration inhibited the activation of p38 MAPK activity at 41 C to 127± 21 % of that at 37 C. Our results indicate acomplex interactionbetweenheat stress and oxidative stress on activation of p38 MAPK in heart. Suppression of p38 MAPK activity by pretreatment with antioxidant may be one strategy for organ protection against thermal injury in heart.
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