The role of BNIP3L-mediated mitophagy in cadmium-induced apoptosis in rat cerebral cortical neurons
In order to determine the regulatory effect of BNIP3L-mediated mitophagy on apoptosis induced by cadmium(Cd),the rat cere-bral cortical neuron BNIP3L gene silencing model was established,in this study,by RNA interference technique,and then the model was treated with 10μmol/L Cd for 12 h.Next,the expression levels of BNIP3L,Parkinson disease protein 2(Parkin)and mitochondrial apopto-sis pathway-related proteins cleaved caspase-9 and cleaved caspase-3 were detected by Western blot.The co-localization of BNIP3L and the mitochondrial marker protein TOMM20 was detected by immunofluorescence staining.And,transmission electron microscopy was used to determine the number of mitophagosomes in neurons.Finally,apoptosis was detected by FITC Annexin V staining.The results showed that the expression of BNIP3L was significantly increased(P＜0.01),and the co-localization of BNIP3L and TOMM20 was increased after Cd treatment for 12 h.Silencing BNIP3L significantly inhibited Cd-induced Parkin translocation to mitochondria(P＜0.01),inhibited Cd-in-duced mitophagosome formation,and significantly promoted Cd-induced caspase-9 and caspase-3 activation and neuronal apoptosis(P＜0.01).The present results indicated that BNIP3L-mediated mitophagy was able to inhibit Cd-induced apoptosis in rat cerebral cortical neurons.
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维普
