Silymarin augments human cervical cancer HeLa cell apoptosis via P38/JNK MAPK pathways in serum-free medium

J Asian Nat Prod Res. 2005 Oct;7(5):701-9. doi: 10.1080/1028602042000324862.


Silymarin was proved to have a protective effect of UV-induced A375-S2 cell apoptosis in our previous research. In this study, its pro-apoptotic and anti-apoptotic activities on human cervical cancer (HeLa) cells in vitro were investigated. Silymarin induced HeLa cell death through both apoptotic and necrotic pathways. At low doses (below 80 micromol l-1), it induced cell apoptosis, but caused necrosis at high dose (160 micromol l-1). Silymarin induced typical chromatin condensation and nuclear fragmentation as a hallmark of apoptosis. In this case, mitochondrial Bcl-2 family, Bcl-2 and Bax, were not involved in apoptotic effects; however, silymarin-induced cell death was regulated by the activation of p38 and JNK MAPKs. We also found that pan-caspase inhibitor and caspase-3 inhibitor could not antagonise silymarin-induced apoptosis. Therefore, silymarin induced and augmented HeLa cell apoptosis through p38/JNK MAPKs in the serum-free medium.

MeSH terms

  • Apoptosis / drug effects*
  • Blotting, Western
  • Culture Media, Serum-Free
  • HeLa Cells
  • Humans
  • MAP Kinase Kinase 4 / metabolism*
  • MAP Kinase Signaling System / drug effects*
  • Silymarin / pharmacology*
  • p38 Mitogen-Activated Protein Kinases / metabolism*


  • Culture Media, Serum-Free
  • Silymarin
  • p38 Mitogen-Activated Protein Kinases
  • MAP Kinase Kinase 4