To evaluate the growth inhibition effect of AMDT on various human tumor cells, the cells were treated with AMDT for 24 h.
Table 1 Growth inhibition of AMDT on various human cell lines (24 h).
Cell cycle distribution and induction of apoptosis of 95-D cells under AMDT treatment
To elucidate whether the decrease in cell viability induced by AMDT was attributable to apoptosis, nuclear staining with Hoechst 33258 and annexin V/PI staining were conducted.
By contrast, the condensation of nuclei and bleb-bing characteristic of apoptotic cells were evident in 95-D cells treated with different concentrations AMDT or positive control HCPT (Fig.
Table 2 Effects of AMDT on apoptosis and necrosis of 95-D human lung tumor cells (HCPT as positive control).
Effect of AMDT on mitochondrial transmembrane potential ([DELTA][psi]/m) and caspase-3 and -9 activities
To evaluate the influence of AMDT on the function of mitochondria, alterations in mitochondrial potential were analyzed by employing a fluorescent dye Rh123.
Following 24 h treatment of 95-D cells with various concentrations of AMDT, significant increases of both caspase-9 and -3 activities were detected and found to be in a dose-dependent manner compared with the control (Fig.
In this study, the new acyclic sesquiterpene AMDT from the hairy root cultures of A.
The growth inhibitory effect of AMDT on 95-D cells (Fig.
Further experiments revealed that apoptosis and cell cycle progression block were both responsible for the inhibition of the tumor cell proliferation by AMDT.