Conclusion
Taken together, our studies demonstrate that Triphalainduced
apoptosis in human pancreatic cancer cells is
mediated by the activation of ERK and p53, which in turn
is initiated by ROS generation. Moreover, oral administration
of Triphala significantly suppress the growth of pancreatic
tumor xenograft in nude mice by inducing
apoptosis and activation of ERK and p53 in the tumor
cells, a mechanism similar to that we observed in vitro.
Our results thus provide a rationale for the development
of Triphala as chemopreventive or chemotherapeutic
agent against pancreatic cancer in the clinical practice.