[6]-
Gingerol, a pharmacologically important bioactive component of ginger, has been reported to have anti-hyperglycemic, anti-
cancer and anti-oxidative properties, but mechanisms through which these are achieved are largely unclear. The present study focuses on apoptosis and autophagy, two key events of anti-
cancer activity, in HeLa cells treated with [6]-
gingerol. The treated cells showed several morphological changes, including externalization of
phosphatidyl serine, degradation of
DNA and increase in TUNEL positivity. Furthermore, there was depolarization of mitochondrial membrane potential, providing evidence of mitochondria mediated apoptosis. The expression of
caspase 3 and PARP was increased in cells exposed to [6]-
gingerol. Circular dichroism study for testing
drug-
DNA interaction with both calf thymus and nuclear
DNA as target revealed that the
drug had potential to bind with the nuclear
DNA and induce conformational changes of
DNA. The over-expression of NFkβ, AKT and Bcl2 genes in
cancer cells was down-regulated by [6]-
gingerol treatment. On the other hand the expression levels of TNFα, Bax and
cytochrome c were enhanced in [6]-
gingerol treated cells. Thus, overall results suggest that [6]-
gingerol has potential to bind with
DNA and induce cell death by autophagy and
caspase 3 mediated apoptosis.