| Project/Area Number |
16591838
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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 |
Morphological basic dentistry
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| Research Institution | Nihon University |
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Principal Investigator |
KURITA-OCHIAI Tomoko Nihon University, School of Dentistry at Matsudo, Lecturer (Full-Time), 松戸歯学部, 講師 (20130594)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2004: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | apoptosis / T cells / Volatile fatty acid / ROS / 酪酸 / 酸化ストレス / ROS |
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| Research Abstract |
1.In the Death/receptor analysis through TNFα, butyric acid suppressed the transcript revitalization of c-FLIP. As the result, the caspase-8 was activated decreasing in the amount of the c-FLIP protein, followed by apoptosis was induced to T cells. It seems that the increase of TNFα and TNFβ by butyric acid induces the appearance of TNFR and advances to the activation of caspase-8 with a decrease of FLIP.
2.In butyric acid-induced T cell apoptosis, it has been thought that (1)Increases of Cytochrome c, Apaf 1 and Smac expressions according to an increase in mitochondria membrane potential and (2)Appearance change of Bcl-family proteins with action part in mitochondrial membrane, were the main part of the apoptosis execution signal through mitochondoria. However, our result in this time indicated that butyric acid-induced apoptosis was deeply related to caspase-8 and -12 than caspase-3 and -9 which working at the downstream of mitochondria. The participation of caspase-8 and -10 suggests that the Death ligand/receptor system through above-mentioned TNFα is induced with butyric acid, while the participation of caspase-12 strongly suggests the butyric acid is taking part in apoptosis for which uses endoplasmic reticula in the cell.
3.In addition, it is thought that ROS also influences in organelles other than caspase-3 and -9 that works in relation to mitochondria. The finding to which an increase of p38 with butyric acid is remarkably controlled with an anti-oxidant establishes the thioredoxin-ASK1 complex is controlling ROS-related p38 MAPK route in the aging mouse.
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