Ogata S, Takeuchi M, Okumura K, Taguchi H
Laboratory of Biological Chemistry, Faculty of Bioresouces, Mie University, Japan.
Biosci Biotechnol Biochem. 1998 Dec;62(12):2351-6. doi: 10.1271/bbb.62.2351.
We have investigated whether niacin-related compounds act as inducers of apoptosis in HL-60 cells. In this study, we found that picolinic acid, dipicolinic acid, and isonicotinamide strongly induce apoptosis. After treatments with these compounds, apoptosis started within 4 h and was induced in about 50% of the cells within 8 h. These compounds induced apoptosis at 5-10 mM, but did not at 1 mM. An ICE-like protease inhibitor (Z-Asp-CH2-DCB) completely blocked the apoptosis, but a caspase-1 inhibitor (Ac-YVAD-CHO) and a caspase-3 inhibitor (Ac-DEVD-CHO) did not block the apoptosis, suggesting that other caspases have the critical roles in the execution process of apoptosis induced by niacin-related compounds.
我们研究了烟酸相关化合物是否可作为HL-60细胞凋亡的诱导剂。在本研究中,我们发现吡啶甲酸、二吡啶甲酸和异烟酰胺可强烈诱导凋亡。用这些化合物处理后,凋亡在4小时内开始,8小时内约50%的细胞被诱导凋亡。这些化合物在5-10 mM时诱导凋亡,但在1 mM时不诱导。一种ICE样蛋白酶抑制剂(Z-Asp-CH2-DCB)完全阻断了凋亡,但半胱天冬酶-1抑制剂(Ac-YVAD-CHO)和半胱天冬酶-3抑制剂(Ac-DEVD-CHO)并未阻断凋亡,这表明其他半胱天冬酶在烟酸相关化合物诱导的凋亡执行过程中起关键作用。