Silymarin augments human cervical cancer HeLa cell apoptosis via P38/JNK MAPK pathways in serum-free medium.
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.
Huang
Qing
Q
China-Japan Research Institute of Medical and Pharmaceutical Sciences, Shenyang Pharmaceutical University, China.
Wu
Li-Jun
LJ
Tashiro
Shin-Ichi
S
Onodera
Satoshi
S
Li
Lin-Hao
LH
Ikejima
Takashi
T
D017209:Apoptosis / Q000187:drug effects*; D015153:Blotting, Western; D016895:Culture Media, Serum-Free; D006367:HeLa Cells; D006801:Humans; D048670:MAP Kinase Kinase 4 / Q000378:metabolism*; D020935:MAP Kinase Signaling System / Q000187:drug effects*; D012838:Silymarin / Q000494:pharmacology*; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism*
D016895:Culture Media, Serum-Free; D012838:Silymarin; D048051:p38 Mitogen-Activated Protein Kinases; D048670:MAP Kinase Kinase 4