Document Detail


Swainsonine Induces Caprine Luteal Cells Apoptosis via Mitochondrial-Mediated Caspase-Dependent Pathway.
MedLine Citation:
PMID:  24977789     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Swainsonine (SW) is an indolizidine alkaloid isolated from a number of poisonous plants. We have previously reported that SW inhibited luteal cell progesterone production by inducing caprine luteal cell apoptosis in vitro; however, the molecular mechanism of this phenomenon remains unclear. In this study, SW-treated luteal cells showed apoptosis characteristics, including nuclear fragmentation, DNA ladder formation, and phosphatidylserine externalization. Further studies showed that SW activated caspase-9 and caspase-3, which subsequently cleaved poly(ADP-ribose) polymerase. SW also increased in Bax/BcL-2 ratios, promoted Bax translocation from the cytosol to mitochondria, and triggered the release of cytochrome c from mitochondria into the cytoplasm. However, Fas and Fas ligand induction or caspase-8 activity did not appear any significant changes. Additional analysis also showed that pan-caspase inhibitor, caspase-9 inhibitor, or caspase-3 inhibitor almost completely protected the cells from SW-induced apoptosis, but not caspase-8 inhibitor. Overall, these data demonstrated that SW induced luteal cells apoptosis through a mitochondrial-mediated caspase-dependent pathway.
Authors:
Wei Li; Yong Huang; Xiaomin Zhao; Wenlong Zhang; Feng Dong; Qian Du; Dewen Tong
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-6-30
Journal Detail:
Title:  Journal of biochemical and molecular toxicology     Volume:  -     ISSN:  1099-0461     ISO Abbreviation:  J. Biochem. Mol. Toxicol.     Publication Date:  2014 Jun 
Date Detail:
Created Date:  2014-6-30     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9717231     Medline TA:  J Biochem Mol Toxicol     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
© 2014 Wiley Periodicals, Inc.
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