Abstract:
:Propofol has been shown to attenuate brain injury in experimental ischemia models, but few studies have focused on the direct effect of propofol on mitochondrial dysfunction. In this study, we observed the effects of propofol on multiple aspects of mitochondrial dysfunction by studying the mitochondria isolated from rat brains subjected to focal cerebral ischemia-reperfusion. The mitochondria of the cortical tissue were isolated by the Percoll density gradient centrifugation. The isolated mitochondria were fixed and examined with electron microscopy. The calcium-induced mitochondrial swelling was quantified by measuring the decrease in light transmission at 540 nm with a spectrometer. Fluorescent probes were used to selectively stain mitochondria. Flow cytometry was used to measure the membrane potential and the production of reactive oxidative species. Propofol improved the signs of injury in the cortical mitochondria that were exposed to reperfusion following 2 h of focal ischemia. Propofol prevented calcium-induced mitochondrial swelling in a concentration-dependent manner. It did not affect the reperfusion-induced reduction in mitochondrial membrane potential. However, it decreased the production of the mitochondrial reactive oxidative species, which are generated during reperfusion. These results demonstrate that propofol may protect against mitochondrial dysfunction by preventing the ultrastructural change to the mitochondria and the calcium-induced mitochondrial swelling. This protective effect may be mediated by inhibiting the mitochondrial membrane permeability transition and reducing the production of reactive oxidative species in mitochondria.
journal_name
Neuropharmacologyjournal_title
Neuropharmacologyauthors
Li J,Yu W,Li XT,Qi SH,Li Bdoi
10.1016/j.neuropharm.2013.08.029subject
Has Abstractpub_date
2014-02-01 00:00:00pages
358-68eissn
0028-3908issn
1873-7064pii
S0028-3908(13)00396-1journal_volume
77pub_type
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