Dihydroartemisinin transiently activates the JNK/SAPK signaling pathway in endothelial cells.

摘要: Artemisinin and its derivatives are well-known anti-malaria drugs in the early stages of research for cancer treatment. Dihydroartemisinin (DHA), a more water-soluble derivative artemisinin, has demonstrated strong anti-angiogenic activity. The purpose present study was to investigate underlying molecular mechanisms effect DHA on angiogenesis. Human umbilical vein endothelial cells (HUVECs) treated with were examined apoptosis activation c-Jun N-terminal kinase (JNK) signaling pathway, one major mitogen-activated protein cascades. It observed that 20 µM induces transient JNK HUVECs. also elevates expression cyclooxygenase-2 matrix metalloproteinase-13, which is abolished by treatment inhibitor SP600125. Although persistently increases κB-α thus inhibits nuclear factor-κB signaling, it does not affect or caspase 3/9 activities provides key information understanding effects cells, required investigating potential clinic application as chemotherapeutic agent.