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通过对Ridaifen-G(RID-G)诱导造血细胞U937、Raji、THP-1和IM-9死亡是否需要Z-VAD-fmk(一种细胞凋亡蛋白酶抑制剂)的研究,发现RID-G以细胞凋亡蛋白酶非依存性的方式诱导细胞死亡,并伴随有线粒体功能紊乱。Z-VAD-fmk对U937细胞的死亡没有影响,但抑制etoposide诱导的细胞凋亡;DNA片段化结果表明,RID-G可破坏Raji和THP-1细胞的DNA,经RID-G处理后的U937细胞的DNA条带没有经etoposide处理的清晰。此外,Z-VAD-fmk对U937、THP-1和Raji细胞DNA的片段化程度有不同的影响,抑制细胞死亡。这些结果表明,RID-G诱导的非典型细胞死亡不依赖于caspase,且伴随有线粒体功能紊乱。
A study of whether Z-VAD-fmk, an inhibitor of apoptosis protein, is required for the death of hematopoietic cells U937, Raji, THP-1 and IM-9 by Ridaifen-G (RID- Apoptotic protease-independent manner induces cell death accompanied by mitochondrial dysfunction. Z-VAD-fmk had no effect on the death of U937 cells but inhibited etoposide-induced apoptosis. The results of DNA fragmentation showed that RID-G could destroy the DNA of Raji and THP-1 cells. The RID-G treated U937 Cell DNA bands were not clearly treated with etoposide. In addition, Z-VAD-fmk has different effects on the degree of DNA fragmentation of U937, THP-1 and Raji cells and inhibits cell death. These results indicate that RID-G-induced atypical cell death is independent of caspases and is accompanied by mitochondrial dysfunction.