EFFECT OF NON-STEROIDAL ANTI-INFLAMMATORY DRUGS ON THE EXPRESSION OF GROWTH FACTORSAND THEIR RECEPTORS
Grant-in-Aid for Scientific Research (C)
|Research Institution||SAITAMA MEDICAL SCHOOL|
OTA Shinichi SAITAMA MEDICAL SCHOOL,MEDICAL DEPARTMENT,ASSINTANT PROFESSOR, 医学部, 助教授 (30185269)
|Project Fiscal Year
1996 – 1997
Completed(Fiscal Year 1997)
|Budget Amount *help
¥2,200,000 (Direct Cost : ¥2,200,000)
Fiscal Year 1997 : ¥1,100,000 (Direct Cost : ¥1,100,000)
Fiscal Year 1996 : ¥1,100,000 (Direct Cost : ¥1,100,000)
|Keywords||NSAID / PROSTAGLANDIN / HEPATOCYTE GROWTH FACTOR / HUMAN FIBLOBLAST / CYCLOOXYGENASE / プロスタグランジン / 肝細胞増殖因子 / 人線維芽細胞 / シクロオキシゲナーゼ / 人胃・大腸線維芽細胞 / 非ステロイド系消炎鎮痛剤 / COX|
Effects of indomethacin, a NON-STEROIDAL ANTI-INFLAMMATORY DRUG (NSAID), on the expression of hepatocyte growth factor (HGF) were investigated using normal human gastric and colonic fibroblasts. Results are as follows ;
a.Human gastric and colonic fibroblasts produced HGF.
b.Prostaglandins (PGs) stimulated HGF production. The order of potency was PGE1 * PGE2 > PGI2 analogue.
c.Exogenous cAMP and cholera toxin increased HGF production.
d.PGEl increased cellular cAMP.
e.Among FGF,TGFalpha, EGF,TNF-alpha, and IL1-beta, only IL1-beta dramatically increased endogenous PGE2 production.
f.IL1-beta induced not cyclooxygenase (COX)-l but COX-2.
g.Indomethacin completely blocked IL1-beta-induced increase of PGE2.
h.IL1-beta increased HGF,which was prevented by indomethacin.
These results suggest that NSAIDs may inhibit PG-induced increase of HGF production by suppressing endogenous PG production. This may explain in part the mechanisms of gastric injury and suppression of colon carcinogenesis by NSAIDs.
Research Output (3results)