Project/Area Number |
07670681
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Respiratory organ internal medicine
|
Research Institution | Tokyo Women's Medical College |
Principal Investigator |
NAGAI Atsushi Tokyo Women's Medical College, Department of Medicine 1 Professor, 医学部, 教授 (60101820)
|
Co-Investigator(Kenkyū-buntansha) |
KAMEYAMA Shinkichi Tokyo Women's Medical College, Department of Medicine 1 Instructor, 医学部, 助手 (50214557)
YASUI Shuji Tokyo Women's Medical College, Department of Medicine 1 Assistant professor, 医学部, 講師 (30147392)
|
Project Period (FY) |
1995 – 1996
|
Project Status |
Completed (Fiscal Year 1996)
|
Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1996: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1995: ¥1,400,000 (Direct Cost: ¥1,400,000)
|
Keywords | Oxidant / elastase / apoptosis / necrosis / DNA / lung injury / 急性肺傷害 / ネフローシス / レドックスサイクル / ナイアシン / ニコチナマイド / ATP / NAD |
Research Abstract |
1)In vivo experiments (1)An Administration of niacin or nicotinamide inhibited oxidant-induced acute lung injury. (2)Elastase induced detachment of airway epithelium, and SLPI protected the cells from the detachment. (3)Neutrophil sequestration induced by G-CSF did not produce acute inflammation in the lung. (4)P-selectin antagonist inhibited acute lung inflammation induced by LPS. 2)In vitro experiments (1)Oxidant induced necrosis and/or apoptosis in the airway epithelium, and these effects ware in dose-and time-dependent fashion. (2)TNF alpha induced apoptosis in the lung fibroblasts. (3)Depletion of cystine induced apoptosis in the lung fibroblasts and airway epithelium. These findings suggest that intra-celluar reactive oxygen may be associated with signal transduction of apoptosis.
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