| Project/Area Number |
08672212
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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 |
Conservative dentistry
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| Research Institution | KANAGAWA DENTAL COLLEGE |
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Principal Investigator |
HORI Toshio KANAGAWA DENTAL COLLEGE,PERIODONTOLOGY,PROFESSOR., 歯学部, 教授 (80084721)
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| Co-Investigator(Kenkyū-buntansha) |
DEGUCHI Shinji KANAGAWA DENTAL COLLEGE,PERIODONTOLOGY,ASSOCIATED PROFESSOR., 歯学部, 助教授 (60121018)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1997: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1996: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | POLYMORPHONUCLEAR LEUKOCYTE / HUMAN PERIODONTIUM DERIVED CELLS / CYTOTOXICITY / 細胞障害性 |
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| Research Abstract |
The investigation of polymorphonuclear leukocytes (PMNs) mediated damage to periodontium derived cells is important to clear the mechanism of periodontal disease. We recently showed that lipopolysaccharide (LPS) enhanced N-fomil-methionyl-leucyl-phenylalanine (FMLP) stimulated PMNs mediated damage to cultured human periodontal fibroblast (HPLF). Superoxide (O_2^-), H_2O_2, ^-OH,^1O_2 have all been implicated as the toxic agents when cells are exposed to oxygen radicals. The mechanism by which these oxygen radicals cause damage to periodontium derived cells is unknown. It is important to determine which oxygen radicals are responsible for cellular damage in order to elucidate the mechanism of cytotoxicity. The present study was designed to evaluated the effect of these oxygen radicals for PMNs-mediated damage to human gingival derived fibroblast (HGF) and human gingival epithelial cell (HGE). Cells were cultured until confluent monolayr and subjected to LPS (1000ng/ml) and FMLP (10^<-6>M) stimulated PMNs, and then exposed to scavengers of (O_2^-) and H_2O_2. After treatment, the cells were stained to distinguish between normal and damaged cells. The system of LPS and FMLP stimulated PMNs was significantly (p<0.05) increased the percent of damaged HGF and HGE compared with other systems. Superoxide dismutase (SOD) (10mug/ml ; 3,300 U/mg) with or without catalase (100mug/ml ; 6,900 U/mg) had no significant inhibitory effect on PMNs mediated injury of HGF.
These results suggest that, in this system, FMLP and LPS-stimulated PMNs-mediated damage to HGF may not be mediated by O_2^-, H_2O_2. This damage may be mediated in large part by other oxygen radicals and protease are released from PMNs.
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