Ginsenoside Rh1 Improves the Effect of Dexamethasone on Autoantibodies Production and Lymphoproliferation in MRLlpr Mice

الملخص EN

Ginsenoside Rh1 is able to upregulate glucocorticoid receptor (GR) level, suggesting Rh1 may improve glucocorticoid efficacy in hormone-dependent diseases.

Therefore, we investigated whether Rh1 could enhance the effect of dexamethasone (Dex) in the treatment of MRL/lpr mice.

MRL/lpr mice were treated with vehicle, Dex, Rh1, or Dex + Rh1 for 4 weeks.

Dex significantly reduced the proteinuria and anti-dsDNA and anti-ANA autoantibodies.

The levels of proteinuria and anti-dsDNA and anti-ANA autoantibodies were further decreased in Dex + Rh1 group.

Dex, Rh1, or Dex + Rh1 did not alter the proportion of CD4+ splenic lymphocytes, whereas the proportion of CD8+ splenic lymphocytes was significantly increased in Dex and Dex + Rh1 groups.

Dex + Rh1 significantly decreased the ratio of CD4+/CD8+ splenic lymphocytes compared with control.

Con A-induced CD4+ splenic lymphocytes proliferation was increased in Dex-treated mice and was inhibited in Dex + Rh1-treated mice.

Th1 cytokine IFN-γ mRNA was suppressed and Th2 cytokine IL-4 mRNA was increased by Dex.

The effect of Dex on IFN-γ and IL-4 mRNA was enhanced by Rh1.

In conclusion, our data suggest that Rh1 may enhance the effect of Dex in the treatment of MRL/lpr mice through regulating CD4+ T cells activation and Th1/Th2 balance.