Background : Propofol is a short-acting analgesic agent frequently used for intravenous anesthesia. In addition to having an anesthetic function, it has recently been reported to exert a neuro-protective effect during cerebral ischemia reperfusion. Although it has been suggested that propofol suppresses apoptosis in neuronal cells induced by reperfusion of ischemic tissue, much of the neuro-protective mechanism of propofol remains to be clarified. The purpose of this study was to investigate whether propofol affected mitochondrial fragmentation caused by mitochondrial fission, the initial stage of apoptosis. Methods : Human neuroblastoma SH-SY5Y cells were treated with CCCP, an uncoupler, in the presence or absence of propofol. Fragmentation of mitochondria was evaluated by live cell imaging ; cleavage of OPA1, a mitochondrial fusion factor cleaved and generated as a short form (S-OPAl) from a long form (L-OPAl) during mitochondrial fission, was detected by western blotting. Results: Mitochondrial fragmentation induced by CCCP was suppressed by propofol. Moreover, cleavage of L-OPAl to S-OPAl was delayed by the addition of propofol. Conclusion : The present results showed that propofol delayed the fragmentation of mitochondria. This suggests that the neuro-protective function of propofol is due to delayed mitochondrial fragmentation during apoptosis.
|Number of pages||8|
|Journal||Journal of Tokyo Medical University|
|Publication status||Published - Jan 1 2015|
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