Journal
MOLECULES
Volume 19, Issue 10, Pages 15786-15798Publisher
MDPI AG
DOI: 10.3390/molecules191015786
Keywords
pinocembrin; ischemia/reperfusion; penumbra; autophagy
Funding
- National Scientific & Technological Major Project [2012ZX09103-101-078]
- Special Foundation for Scientific Research in Public Health Industry [200902008]
- National Natural Science Foundation of China [81102444]
- Central Public Scientific Research Institution Fundamental Project by Chinese government [2014CX05]
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The aim of this study was to investigate the effects of pinocembrin on brain ischemia/reperfusion (I/R) injury and the potential involvement of autophagy activity changes in the penumbra area in the mechanisms of pinocembrin activity. Focal cerebral I/R model was induced by middle cerebral artery occlusion (MCAO) for 2 h followed by 24 h reperfusion. Pinocembrin was administered intravenously at different doses (1, 3, and 10 mg/kg, respectively) at the onset of reperfusion. Neurological function, brain infarction and brain swelling ratio were evaluated. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) method and immunohistochemical analysis (Caspase-3) were used to evaluate apoptosis in the penumbra cortex. Two key proteins of autophagy, LC3B and Beclin1, were detected by western blot. The results showed that pinocembrin-treatment could significantly reduce neurological deficit scores, infarct volume, cerebral edema and improve pathological lesion in the I/R rats. Pinocembrin-treatment could also reduce the number of TUNEL-positive and Caspase-3-positive neurons, and upregulate the expression of LC3B and Beclin1 in the penumbra area. These results suggested that pinocembrin could protect the brain against I/R injury, and the possible mechanisms might be attributed to inhibition of apoptosis and reversed autophagy activity in the penumbra area.
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