Artesunate induces apoptosis via a ROS-independent and Bax-mediated intrinsic pathway in HepG2 cells

Artesunate induces ROS-dependent apoptosis via a Bax-mediated intrinsic pathway in Huh-7 and Hep3B cells

“…In contrast to our recent finding that ARS induced ROS-independent apoptosis in HepG2 cells [33], we here found that ROS played an important role in ARS-induced apoptosis in both Huh-7 and Hep3B cell lines (Fig. 3), though ARS induced intrinsic apoptosis in which Bax played a key role the three HCC cell lines.…”

“…Although ARS induced ROS generation in HepG2 cells ( Fig.2A), ARS-induced iron homeostasis disturbance preferentially dominated the ARS-induced ROS-independent apoptosis (Fig. 3B), which was consistent with our recent finding [33] and recent report that DHA caused cellular iron depletion and disturbed iron homeostasis in cancer cells independent of oxidative damage [49]. In contrast to HepG2 cells, Huh-7 cells have the lowest basal intracellular iron ions level in the three HCC cell lines ( Fig.…”

“…4D) in both Huh-7 and Hep3B cell lines, indicating the important role of Bax in ARS-induced apoptosis in the two cell lines. The gene silencing efficiency of shBax or shBak was assessed by Western blotting analysis in our previous work [33]. These data demonstrated that ARS induced apoptosis via the Bax-mediated intrinsic pathway in Huh-7 and Hep3B cells.…”

Quercetin attenuates high fructose feeding-induced atherosclerosis by suppressing inflammation and apoptosis via ROS-regulated PI3K/AKT signaling pathway

“…Excessive ROS production promotes the detrimental regulation of important intracellular macromolecules, including proteins, lipids, as well as DNA, leading to apoptosis and inflammatory response [7,8]. The cell apoptosis and inflammation are associated with subsequent plaque formation [9].…”

Markers of oxidative‐nitrosative stress induced by artesunate are followed by clastogenic and aneugenic effects and apoptosis in human lymphocytes

“…In contrast, the mechanisms involved in programmed cell death triggered by ARS in normal control cells is considerably less known (Cheng et al, ). ARS was found to induce apoptotic cell death in several tumor cell lines in a caspase‐independent manner (Greenshields et al, ; Papanikolaou et al, ; Wang et al, ) and in a caspase‐dependent manner, via intrinsic (mitochondrial pathway) and extrinsic pathways (Kim, Lee, Kim, Sethi, & Ahn, ; Li et al, ; Pang et al, ; Qin et al, ; Zhang, Luo, Li, & Tan, ). In this study, an ARS‐induced increase of caspases 8 and 9 and cytochrome c expression may suggest that both the mitochondrial and death receptor apoptotic pathways are likely to be activated in non‐tumor cell death following ARS exposure.…”