Study on Mitochondria Signal Transduction Pathway of Apoptosis for SGC-7901 Induced by CSBE

Abstract

In order to study mitochondria signal transduction pathway of apoptosis of SGC-7901 induced by n-butanol extract from Capparis spionosa L. (CSBE), effect of apoptosis of SGC-7901 induced by CSBE was observed. In addition, the changes of initiator, effector and marker in process of mitochondria signal transduction pathway were surveyed. The inhibitory and killing effects of SGC-7901 induced by CSBE were studied by MTT method, and apoptosis of SGC-7901 induced by CSBE was observed with flowcytometry. Mitochondrial membrane potential was detected by SRB 123 to reveal initiator in mitochondrial apoptosis pathway induced by CSBE. The release of cytochrome C (Cyt c), marker of mitochondrial apoptosis pathway, was analyzed with western blot method. Activity of caspase 3 which was the effector of mitochondrial apoptosis pathway was measured by enzyme-labeled instrument. CBSE can inhibit growth of SGC-7901, and induce apoptosis. Proportion of apoptotic cell was increased as concentration of drug rised. CSBE could reduce mitochondrial membrane potential and initiate mitochondrial apoptosis pathway. After SGC-7901 was treated with CSBE, the up-regulation of expression of Cyt c in cytoplasm indicated that Cyt c was involved in apoptosis process induced by CSBE. CSBE could activate caspase-3, effector of mitochondrial apoptosis pathway, which caused apoptosis of SGC-7901. As a result, CSBE can induce mitochondrial PTP channel open of SGC-7901, and decrease mitochondrial membrane potential. In addition, CSBE could result in release of mitochondrial Cyt c, and cause activation of Caspase-3. Eventually SGC-7901 was induced apoptosis through mitochondrial signal transduction pathway.