Coompo Research Chemicals

Saikosaponin-D (SSd) significantly reduced collagen I deposition in the liver and alanine aminotransferase level in the serum. Moreover, SSd decreased the content of TGF-beta1 in the liver, which was significantly elevated after dimethylnitrosamine induced liver fibrosis. Furthermore, SSd was able to alleviate hepatocyte injury from oxidative stress. In conclusion, SSd could postpone the development of liver fibrosis by attenuating hepatocyte injury.

SSd inhibits cell growth of human cancer cells by inducing apoptosis and blocking cell cycle progression in the G1 phase. SSd was found to stimulate corticotropin-releasing factor (CRF) gene expression and CRF release. ELISA assay showed that Saikosaponin D significantly increased the expression of p53 and p21/WAF1 protein, contributing to cell cycle arrest. An enhancement in Fas/APO-1 and its two form ligands, membrane-bound Fas ligand (mFasL) and soluble Fas ligand (sFasL), as well as Bax protein, was responsible for the apoptotic effect induced by Saikosaponin D. Taken together,our study suggests that the induction of p53 and activity of the Fas/FasL apoptotic system may participate in the antiproliferative activity of Saikosaponin D in A549 cells.

Pretreatment with SSd produced a remarkable inhibitory action on acute hepatic injury by CCl4. A significant inhibition of lipid peroxidation induced by an acute dose of CCl4 in the liver of rats pre-treated with SSd was also noted. Continuous injection of CCl4 caused liver cirrhosis in rats but the severity of cirrhosis was reduced in rats treated simultaneously with CCl4 and SSd.