College of Oriental Medicine, Kyung Hee University, Seoul 130-701, South Korea.
Cancer Lett. 2010 Dec 8;298(2):212-21. doi: 10.1016/j.canlet.2010.07.007. Epub 2010 Jul 31.
We demonstrate that decursin induces apoptosis via regulation of cyclooxygenase-2 (COX-2) and survivin in leukemic KBM-5 cells. By activating an apoptotic machinery, decursin is cytotoxic to KBM-5 cells. In this apoptotic process, decursin can activate caspase family members and triggers PARP cleavage. At the same time, the expression of COX-2 and survivin in the cells is downregulated. Furthermore, decursin is in synergy with COX-2 inhibitor, celecoxib or NS398 for the induction of apoptosis. Overall, these results suggest that decursin, via inhibiting COX-2 and survivin, sensitizes human leukemia cells to apoptosis and is a potential chemotherapeutic agent to treat this disease.
我们证明了蛇床子素通过调节环氧化酶-2(COX-2)和存活素诱导白血病 KBM-5 细胞凋亡。蛇床子素通过激活凋亡机制对 KBM-5 细胞具有细胞毒性。在这个凋亡过程中,蛇床子素可以激活半胱天冬酶家族成员并触发 PARP 切割。同时,细胞中 COX-2 和存活素的表达下调。此外,蛇床子素与 COX-2 抑制剂塞来昔布或 NS398 协同诱导细胞凋亡。总的来说,这些结果表明,蛇床子素通过抑制 COX-2 和存活素使人类白血病细胞对凋亡敏感,是治疗这种疾病的一种潜在化疗药物。