Extract of Myrica cerifera bark has long been fruitfully used as a hepato-protective and anti-
cancer drug in various complementary and alternative systems of medicine.
Myricanone, its principal bioactive compound, had also been reported to have apoptosis-promoting ability. We evaluated its anti-
cancer potential in vitro in HepG2
liver cancer cells and tried to understand the signal cascades involved in accomplishing apoptosis. Further, we ascertained by using a (3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium
bromide assay (MTT) assay if it had cytotoxic effects on normal noncancerous liver cells (WRL-68). We deployed various tools and protocols, like phase contrast, scanning electron and fluorescence microscopies, performed an annexinV-
FITC/PI assay and cell cycle analysis, and estimated the
reactive oxygen species (ROS) generation and mitochondrial membrane depolarization through flow cytometry. Further, analyses of
cytochrome-c translocation and of HSP70 and
caspase expressions were also done by using immunoblota and
Enzyme linked
immunosorbent assay (ELISA). Results revealed that
myricanone induced apoptosis in HepG2 cells through generation of ROS, depolarization of the mitochondrial membrane, early release of
cytochrome-c, down-regulation of HSP70 and activation of a
caspase cascade; it had no, or insignificant, cytotoxic effects in WRL-68 cells in vitro and in mice in vivo. Thus,
myricanone has great potential for use in formulating an effective
drug against both hepatotoxicity and
hepatocellular cancer.