DHA (Dihydroartemisinin)

Dihydroartemisinin (DHA) inhibits the growth of certain cancer cell lines and xenograft tumors such as leukemia, glioma, fibrosarcoma, and breast, cervical, ovarian, lung, oral and pancreatic cancer. DHA inhibits cell and tumor growth by modulating various tumor-suppressive pathways, such as inhibiting cell proliferation and inducing apoptosis through regulation of proliferation- and apoptosis-related proteins.DHA inhibits the proliferation and viability of cells in a dose-dependent manner and induces apoptosis.DHA-mediated cytotoxicity is tumor selective. The endoperoxide bridge of DHA is reportedly essential for its cytotoxicity because it reacts with intracellular ferrous iron to generate reactive oxygen species or carbon-centered radicals, leading to cytotoxicity^[1].

BxPc3-RFP cells (3.5×104cells/well) were seeded in poly D-lysine-coated black, μClear 96-well plates with 0.2 ml medium. After 24 h, the cells were treated with dimethyl sulfoxide (DMSO) (control) or different concentrations (2.5, 10, 40, or 80 μM) of DHA dissolved in DMSO for 24, 48, and 72 h. At each time point, the fluorescence intensity emitted from cells was measured.

DHA significantly inhibited HCC cell growth in vitro and in vivo via inducing G2/M cell cycle arrest and apoptosis^[2].

DHA has been shown in the rat whole embryo culture (WEC) to primarily affect primitive red blood cells (RBCs) causing subsequent tissue damage and dysmorphogenesis^[3].