Skip to main content
eScholarship
Open Access Publications from the University of California

UC Merced

UC Merced Previously Published Works bannerUC Merced

The influence of astragalus polysaccharide and β-elemene on LX-2 cell growth, apoptosis and activation.

  • Author(s): Zheng, Jin
  • Ma, Li-tian
  • Ren, Qin-you
  • Li, Lu
  • Zhang, Yi
  • Shi, Heng-jun
  • Liu, Yi
  • Li, Cheng-hua
  • Dou, Yong-qi
  • Li, Shao-dan
  • Zhang, Hui
  • Yang, Ming-hui
  • et al.
Abstract

Background

Activated hepatic stellate cells are the main source of excessive collagen deposition in liver fibrosis. Here we report the inhibitory effects of the combinational treatment of two natural products, astragalus polysaccharide (APS) and β-elemene (ELE) on the activation of human liver hepatic stellate cell line LX-2 cells.

Methods

Cultured LX-2 cells were treated with different concentrations of APS or ELE for 24 or 48 hours. Cell viability/apoptosis was measured by MTT assay and Annexin V/PI staining , activation related genes including α-SMA and CD44 expressions were measured by real-time PCR and western blot respectively.

Results

The majority of LX-2 cells showed morphological change in the presence of APS or ELE for 24 hours. Treatment with APS + ELE for 24 or 48 hours significantly inhabited the cell proliferation compared with APS or ELE treatment alone on LX-2 cells. APS + ELE may block the up-regulation of α-SMA and CD44 both in mRNA and protein levels through TGF-β pathway in LX-2 cells.

Conclusion

APS or ELE treatment alone on LX-2 cells could inhibit cell proliferation and induce apoptosis. The combinational treatment using APS + ELE significantly increased the killing efficiency on LX-2 cells. α-SMA and CD44 expressions was inhibited upon APS + ELE treatment through TGF-β pathway in LX-2 cells. The results indicated a novel treatment using natural products for liver diseases with anti-fibrotic effect.

Many UC-authored scholarly publications are freely available on this site because of the UC's open access policies. Let us know how this access is important for you.

Main Content
Current View