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N-Butanol Extract of Capparis spinosa L. Induces Apoptosis Primarily Through a Mitochondrial Pathway Involving mPTP Open, Cytochrome C Release and Caspase Activation

  • Ji, Yu-Bin (Center of Research and Development on Life Sciences and Environmental Sciences, Harbin University of Commerce) ;
  • Yu, Lei (Center of Research and Development on Life Sciences and Environmental Sciences, Harbin University of Commerce)
  • Published : 2014.11.28

Abstract

Background: Capparis spinosa L., a Uygur medicine, had been shown to have anti-tumor activity in our early experiments with an N-butanol extract (CSBE) as its active fraction. However, the mechanisms responsible for its effects are not clearly understood. Here, we report that treatment of SGC-7901 cells with CSBE resulted in dose-dependent reduction of cell viability and induction of apoptosis. Materials and Methods: To observe the inhibitory and killing effects of CSBE on SGC-7901, the SRB method was adopted, apoptosis being observed by electron microscopy. To clarify the mechanisms of apoptosis, Western blot and enzyme-labeled methods were used to examine the release of cytochrome c (Cyt c) and the activation of the caspase cascade. Results: By electron microscopy, apoptotic morphologic changes were detectable after CSBE administration. In this study, it was also demonstrated that CSBE induced apoptosis in SGC-7901 cells by inhibiting mPTP open, mitochondrial cytochrome c release, caspase-9 and caspase-3 activation. Conclusions: The findings indicated that CSBE induces aap optosis through mitochondrial pathway.

Keywords

References

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