Anticancer Effects of Eleven Triterpenoids Derived from Antrodia camphorata

YI-PANG LEE; WAN-CHI TSAI; CHIH-JAN KO; YERRA KOTESWARA RAO; CHIUNG-RU YANG; DAR-REN CHEN; MING-HUI YANG; CHI-CHIANG YANG; YEW-MIN TZENG

Figure 1.
Chemical structures of triterpenoid compounds 1-11 isolated from the fruiting bodies of Antrodia camphorata.
Figure 2.
Morphological change in PC-3 cells induced by treatment with triterpenoid compounds 1-11. PC-3 cells were treated with different compounds for 24 hours. Cell morphology was observed under optical microscopy at ×100 (A) and ×200 (B) magnification. Ctrl: DMSO vehicle control; Camp.: camptothecin, positive control. For compound names, see legend to Figure 1.
Figure 3.
Effects of triterpenoid compounds 1-11 on caspase-3 activity in PC-3 cells. PC-3 cells were treated with 50 μM of each compound or camptothecin (Camp.), which served as the positive control. Flow cytometric analysis was carried out after 24-h treatment in order to determine the caspase-3 activity. DMSO served as the vehicle control. For compound names, see legend to Figure 1.
Figure 4.
Effect of methyl antcinate A on apoptosis regulatory proteins. PC-3 cells were treated with 25 μM, 50 μM, and 100 μM of MAA or vehicle control (DMSO) for 6 h. Equal amounts of cell lysates were analyzed for Bcl-2, Bax, and PARP protein expression by western blotting with corresponding antibodies. β-Actin served as the loading control. The values are fold intensity of protein bands of MAA-treated PC-3 cells compared to the respective DMSO vehicle-treated control after being normalized to the respective internal reference (β-actin). The values in the third row denote the relative expression of full-length PARP but not cleaved PARP.