Iwasaki K, Izawa M, Mihara M
Department of Dermatology, School of Life Science, Faculty of Medicine, Tottori University, Yonago, Japan.
Biochem Mol Biol Int. 1997 Sep;42(6):1271-9. doi: 10.1080/15216549700203741.
Six hours after ultraviolet B (UVB) irradiation (11.6 mJ/cm2), the viability of A431 cells decreased, and, at the same time, fragmentation of genomic DNA into nucleosomal units was observed. Z-Asp-CH2-DCB (100 microM), an inhibitor of interleukin-1 beta-converting enzyme (caspase-1) and caspase-1-like proteases, markedly inhibited UVB-induced cell death and DNA fragmentation. Both YVAD-CMK, an inhibitor of caspase-1, and DEVD-CHO, an inhibitor of caspase-3, moderately inhibited the UVB-induced cell death. A combination of YVAD-CMK and DEVD-CHO acted additionally in inhibiting cell death. These observations suggest strongly the cooperative involvement of caspases in the apoptosis induced in A431 cells by UVB.
紫外线B（UVB）照射（11.6 mJ/cm2）6小时后，A431细胞的活力下降，同时观察到基因组DNA断裂成核小体单位。白细胞介素-1β转换酶（半胱天冬酶-1）和类半胱天冬酶-1蛋白酶的抑制剂Z-Asp-CH2-DCB（100 microM）显著抑制UVB诱导的细胞死亡和DNA断裂。半胱天冬酶-1的抑制剂YVAD-CMK和半胱天冬酶-3的抑制剂DEVD-CHO均适度抑制UVB诱导的细胞死亡。YVAD-CMK和DEVD-CHO联合使用对细胞死亡的抑制作用更强。这些观察结果强烈表明，半胱天冬酶协同参与UVB诱导的A431细胞凋亡。
