Journal
MOLECULAR NEUROBIOLOGY
Volume 52, Issue 1, Pages 601-609Publisher
SPRINGER
DOI: 10.1007/s12035-014-8882-7
Keywords
Global cerebral ischemia; PPAR alpha; Fenofibrate; Microglia; P65 NF-kappa B; P38MAPK
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Funding
- National Natural Science Foundation of China [81371217, 30900728, 81472999, 81272350, 81473014]
- Outstanding Young People Project of Guangdong Province [Yq2013137]
- Natural Science Foundation of Guangdong Province [S2013010015464, S2012010008908]
- Science Foundation of Education Bureau of Guangzhou City [10A156]
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Increasing evidence demonstrates that local inflammation contributes to neuronal death following cerebral ischemia. Peroxisome proliferator-activated receptor alpha (PPAR alpha) activation has been reported to exhibit many pharmacological effects including anti-inflammatory functions. The aim of this study was to investigate the neuroprotective effects of PPAR alpha agonist fenofibrate on the behavioral dysfunction induced by global cerebral ischemia/reperfusion (GCI/R) injury in rats. The present study showed that fenofibrate treatment significantly reduced hippocampal neuronal death, and improved memory impairment and hippocampal neurogenesis after GCI/R. Fenofibrate administration also inhibited GCI/R-induced over-activation of microglia but not astrocytes and prevented up-regulations of pro-inflammatory mediators in hippocampus. Further study demonstrated that treatment with fenofibrate suppressed GCI/R-induced activations of P65 NF-kappa B and P38 MAPK. Our data suggest that the PPAR alpha agonist fenofibrate can exert functional recovery of memory deficits and neuroprotective effect against GCI/R in rats via triggering of neurogenesis and anti-inflammatory effect mediated by inhibiting activation of P65 NF-kappa B and P38 MAPK in the hippocampus, which can contribute to improvement in neurological deficits.
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