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Attribution of Bax and mitochondrial permeability transition pore on cantharidin-induced apoptosis of Sf9 cells. | LitMetric

AI Article Synopsis

Article Abstract

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 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.

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Source
http://dx.doi.org/10.1016/j.pestbp.2017.01.010DOI Listing

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