TJN-331 improves anti-glomerular basement membrane nephritis by inhibiting the production of intraglomerular transforming growth factor-β1

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  • Saegusa Yayoi
    Tsumura Research Laboratories, Tsumura & Co. Department of Pathophysiology and Therapeutics, Division of Pharmasciences, Faculty of Pharmaceutical Sciences, Hokkaido University
  • Sadakane Chiharu
    Tsumura Research Laboratories, Tsumura & Co. Department of Pathophysiology and Therapeutics, Division of Pharmasciences, Faculty of Pharmaceutical Sciences, Hokkaido University
  • Koseki Junichi
    Tsumura Research Laboratories, Tsumura & Co.
  • Hasegawa Yoshihiro
    Tsumura Research Laboratories, Tsumura & Co.
  • Shindo Shoichiro
    Tsumura Research Laboratories, Tsumura & Co.
  • Maruyama Hirobumi
    Iwaki Meisei University
  • Takeda Shuichi
    Tsumura Research Laboratories, Tsumura & Co.
  • Takeda Hiroshi
    Department of Pathophysiology and Therapeutics, Division of Pharmasciences, Faculty of Pharmaceutical Sciences, Hokkaido University
  • Hattori Tomohisa
    Tsumura Research Laboratories, Tsumura & Co.

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タイトル別名
  • TJN-331 Improves Anti-glomerular Basement Membrane Nephritis by Inhibiting the Production of Intraglomerular Transforming Growth Factor-.BETA.1
  • TJN 331 improves anti glomerular basement membrane nephritis by inhibiting the production of intraglomerular transforming growth factor v 1

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Transforming growth factor-β1 (TGF-β1) plays an important role in the development of glomerulonephritis. The study of experimental glomerulonephritis in rats was performed to examine the antinephritic effects of TJN-331, a new herbally-derived chemical compound. To clarify the action of TJN-331 ((E)-N-(3,4-dimethoxyphenethyl)-N-methyl-3-(3-pyridyl)-2-propenamide) on TGF-β1 production, glomeruli were isolated from rats with antiglomerular basement membrane (GBM) nephritis and incubated for 48 h with test drugs in vitro. Next, we examined the effects of TJN-331 on rat anti-GBM nephritis induced by injection with anti-GBM serum. TJN-331 dose-dependently inhibited the increase in total and mature TGF-β1 production from nephritic glomeruli, although it did not inhibit TGF-β1 production from normal glomeruli. Administration of TJN-331, at a dose of 2 mg/kg/d, per os (p.o.), prevented proteinuria and increased crescent formation and adhesion of capillary walls to Bowman's capsule. The increases in mature TGF-β1 protein production and TGF-β1 staining score in nephritic rats were reversed by TJN-331 treatment. These results suggest that TJN-331 inhibits proteinuria and histopathological changes in glomeruli via suppression of TGF-β1 production from inflamed glomeruli.

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