Peroxisome proliferator activated receptors (PPAR) α regulates lipid homeostasis and is a target of fibrates, which have a neuroprotective function by various mechanisms. In this study, we aimed to evaluate the role of the PPARα agonist, fenofibrate, in the modulation of cleaved caspase-3 immunoreactivity and at the final infarct volume in an experimental ischemia/reperfusion rat model by induced transient proximal middle cerebral artery occlusion.
Material and Methods:
65 male Spraque Dawley rats were allocated to 4 groups; sham (n = 5), experiment 1 (n = 20), experiment 2 (n = 20), experiment 3 (n = 20). All experiment groups were divided to 3 subgroups in order to evaluate the final infarct volume at 24th hour (n=5) and the immunoreactivity of cleaved caspase -3 at different time period [at first hour (n=5), at 6th (n=5), at 24th (n=5)] after transient middle cerebral artery occlusion (MCAo). At the study the experiment groups (Experiment 1 and Experiment 2) were received the fenofibrate-diet during 14 days before ischemia procedure. All animals were sacrificed at 24th hours after MCAo. Infarction volumes were calculated from 2,3,5,triphenyltetrozolium chloride (TTC)- stained brain sections.Results:
We investigated that fenofibrate-therapy reduced significantly body weight rather than the other experiment groups (p<0.05). At the time intervals, the decrease of immunoreactivity of cleaved caspase-3 significantly observed by fenofibrate therapy after MCAo (p<0.05). Chronic fenofibrate treatment before cerebral ischemia significantly reduced infraction size after MCAo compared with other groups (respectively; p = .011 and p< .000).Conclusion:
The study results supported the neuroprotective effects of fenofibrate treatment in MCA infarcts.