The State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences and Modern Research Center for Traditional Chinese Medicine, Peking University, Beijing 100083, China.
Am J Chin Med. 2006;34(5):887-99. doi: 10.1142/S0192415X06004363.
Previous studies have shown that pseudolaric acid B (PB) would cause apoptosis in human tumor cell lines. However, the mechanisms of PB induced apoptosis are still unclear. In the present study, the mechanisms of PB induced apoptosis in the human hepatocellular carcinoma Bel-7402 cell line were investigated by measuring cell viability, rate of apoptosis, cell cycle, detecting DNA fragmentation, and measuring caspase-3 activation. The results indicated that PB inhibited Bel-7402 cell viability and induced cell death by causing DNA fragmentation, up regulating the early and late apoptotic rates, activating caspase-3 protein, and detaining the cell cycle in the G2/M phases. Additionally, PB-induced apoptosis was a dose- and time-dependent manner. These observations suggest that PB-induced apoptosis occurs through a caspase-dependent pathway and detains the cell cycle in the G2/M phase.
先前的研究表明，土槿皮乙酸 B（PB）会导致人肿瘤细胞系凋亡。然而，PB 诱导凋亡的机制尚不清楚。在本研究中，通过测量细胞活力、凋亡率、细胞周期、检测 DNA 片段化和测量半胱氨酸天冬氨酸蛋白酶-3 的激活，研究了 PB 诱导人肝癌 Bel-7402 细胞系凋亡的机制。结果表明，PB 通过引起 DNA 片段化抑制 Bel-7402 细胞活力并诱导细胞死亡，上调早晚期凋亡率，激活半胱氨酸天冬氨酸蛋白酶-3 蛋白，并将细胞周期阻滞在 G2/M 期。此外，PB 诱导的凋亡呈剂量和时间依赖性。这些观察结果表明，PB 诱导的凋亡是通过半胱氨酸天冬氨酸蛋白酶依赖性途径发生的，并将细胞周期阻滞在 G2/M 期。
