Attribution of Bax and mitochondrial permeability transition pore on cantharidin-induced apoptosis of Sf9 cells.
In: Pesticide Biochemistry & Physiology, Jg. 142 (2017-10-01), S. 91-101
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Zugriff:
To investigate the insecticidal mechanism of cantharidin, a promising biological pesticide substance from blister beetle, on Sf9 cells, a cultured cell line derived from fall armyworm, Spodoptera frugiperda , we preliminary studied the attribution of Bax channel and mitochondrial permeability transition pore on cantharidin-induced mitochondrial apoptosis signal pathway. Changes in cell morphology, activity of mitochondrial dehydrogenases, release of cytochrome C and mitochondrial transmembrane potential were detected when the two channels were blocked by specific inhibitors, Bax channel blocker and cyclosporin A. Results showed that cantharidin-induced apoptotic features, including changes in the cell morphology, release of cytochrome C and decrease in mitochondrial transmembrane potential could be significantly inhibited by Bax channel blocker, while cyclosporin A accelerated the downward trend of mitochondrial dehydrogenases activity and caused a decrease of Ca 2 + in mitochondria. In summary, Bax might be necessary but not exclusively for the apoptosis induced by cantharidin and the attribution of these channels seems to be more complexity. [ABSTRACT FROM AUTHOR]
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Attribution of Bax and mitochondrial permeability transition pore on cantharidin-induced apoptosis of Sf9 cells.
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Autor/in / Beteiligte Person: | Cui, Gaofeng ; Li, Yuansheng ; Ding, Kai ; Hao, Shaodong ; Wang, Jinzhong ; Zhang, Zhiyong |
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Zeitschrift: | Pesticide Biochemistry & Physiology, Jg. 142 (2017-10-01), S. 91-101 |
Veröffentlichung: | 2017 |
Medientyp: | academicJournal |
ISSN: | 0048-3575 (print) |
DOI: | 10.1016/j.pestbp.2017.01.010 |
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