Studies on antinephritc activity of TJC-160

We have already reported that TJC-160, a component of Stachys siebold MIQ(Chorogi) is markedly effective in anti-GBM nephritis and that the antinephritic action of TJC-160 may be partly given by preventing the infiltration of leukocyte via the expression of adhesion moledcule and modulating the activity of metalloproteinase in glomeruli. In the present study, we investigated the effects of TJC-160 on mesangial proliferation in anti-Thy-1 nephritis in rats. TJC-160, prednisolone, captopril was administered orally once a day from the 1st day (exp.1) or 4th day (exp.2) after anti-Thy-1 serum injection, and continued until the end of the experiments. In the experiment 1. TJC-160 improved proteinuria and mesangial proliferation in glomeruli of anti-Thy-1 nephritic rats. TJC-160 suppressed the increase in the number of PCNA or ED-1 positive cells by 50-80%. In addtion, TJC-160 markedly prevented the expression of ICAM-1 in glomeruli. In the experiment 2, although TJC-160 also suppressed the proliferation of mesangal area and the number of PCNA positive cell in glomeruli, TJC-160 failed to prevent the number of ED-1 positive cell and the expression ot ICAM-1 in glomeruli. TJC-160 inhibited the activity of metalloproteinase of glomeruli with anti-Thy-1 nephritic rats. Prednisolone also prevented the mesangial proliferation and the number of PCNA positive cell. However, captopril was not effective in this model. These results indicate that TJC-160 is effective in this model and one of mechanisms of TJC-160 may be the modulation of the expression of adhesion molecules and of metalloproteinase activity.