Studies on the regulatory systems and its physiological significances of the hepatic induction of acute-phase reactants.
Project/Area Number |
63490021
|
Research Category |
Grant-in-Aid for General Scientific Research (B)
|
Allocation Type | Single-year Grants |
Research Field |
広領域
|
Research Institution | Kobe-Gakuin University |
Principal Investigator |
OKAMOTO Hiroshi Kobe-Gakuin University, Faculty of Pharmaceutical Sciences, Professor, 薬学部, 教授 (00028870)
|
Co-Investigator(Kenkyū-buntansha) |
OHTANI Remiko Kobe-Gakuin University, Faculty of Pharmaceutical Sciences, Research Assistant, 薬学部, 実験助手 (00203828)
ITOH Norio Kobe-Gakuin University, Faculty of Pharmaceutical Sciences, Assistant Professor, 薬学部, 助手 (60176352)
|
Project Period (FY) |
1988 – 1989
|
Project Status |
Completed (Fiscal Year 1989)
|
Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 1989: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1988: ¥3,500,000 (Direct Cost: ¥3,500,000)
|
Keywords | Acute-phase reactant / Kininogen / Angiotensinogen / Interleukin-6 / Interferon / 炎症 / 急性期タンパク / キニノーゲン / アンジオテンシノーゲン |
Research Abstract |
(1). Studies on the suppressive and the stimulatory systems in the hepatic production of acute-phase reactant. Production of T-kininogen, a typical acute-phase reactant in the rat, in cultured rat hepatocytes was stimulated by the coculture with activated macrophages or thymocytes. The factors responsible for stimulating hepatic T- kininogen production were identified to be interleukin-6 and interferon-alpha as factors derived from activated macrophages, and interleukin-6 from activated thymocytes. Hepatic T-kininogen production was inhibited by a factor derived from splenic cells, which had previously been activated for a long time by lipopolysaccharide. Macrophages were identified to be cells releasing a suppressive factor, and T cells were required for the induction process of such suppressive macrophages. (2). Inhibitory activity of kininogens an acute-phase reactant on tumor growth. Mouse low-molecular-weight kininogen, as well as rat T-kininogen and egg white cystatin, had the abili
… More
ty to inhibit the growth of tumor cells in vitro. we obtained evidence that the activity was due to inhibition of cathepsin-L- like proteinase by kininogens or cystatin. Kininogens inhibited the growth of tumor cells between G0/G1-phase-and S-phase of cell cycle. (3). Angiotensinogen as an acute-phase reactant. Angiotensinogen level in plasma was increased in the rat by the induction of inflammation. The factor responsible for the acute-phase response was identified to be interleukin-6 by an in vitro experiment using rat hepatoma cells. Inflammation-induced elevation of plasma angiotensinogen caused an increase in plasma renin-activity, suggesting that angiotensin I formation in vivo is enhanced in the inflammatory conditions. In contrast with T-kininogen or alpha_2-macroglobulin, elevation of plasma angiotensinogen was transient even in the condition of chronic inflammation, suggesting that a regulatory system of angiotensinogen production may be different from that of other acute-phase reactants. Less
|
Report
(3 results)
Research Products
(24 results)