Background

Pinocembrin is a major ?avonoid molecule isolated from honey and propolis. It has versatile
pharmacological and biological activities including antimicrobial, anti-in?ammatory, antioxidant, and
anticancer activities as well as neuroprotective effects against cerebral ischemic injury. The purpose of
the current study was to determine the possible mechanisms of neuroprotection elicited by pinocembrin
with speci?c emphasis on chronic prophylactic use before the induction of global cerebral ischemia
reperfusion.

Methods

Global cerebral ischemia–reperfusion was induced by bilateral carotid artery occlusion for
15 min followed by 60 min reperfusion period. Animals were randomly allocated into 3 groups (n = 28):
Sham operated, I/R control and rats treated with pinocembrin (10 mg/kg, po) daily for 7 days then I/R was
induced 1 h after the last dose of pinocembrin. After reperfusion rats were killed by decapitation, brains
were removed and both hippocampi separated and the following biochemical parameters were
estimated; lactate dehydrogenase activity, oxidative stress markers (lipid peroxides, nitric oxide and
reduced glutathione), in?ammatory markers (myeloperoxidase, tumor necrosis factor-alpha, nuclear
factor kappa-B, interleukin-6 and interleukin-10), apoptotic biomarkers (caspase 3 and cytochrome C),
neurotransmitters (glutamate, gamma aminobutyric acid) and infarct size were assessed.
Results: Pinocembrin ameliorated damage induced by I/R through suppressing oxidative stress,
in?ammatory and apoptotic markers as well as mitigating glutamate and lactate dehydrogenase activity.
One of the more signi?cant ?ndings to emerge from this study is that pinocembrin normalized the infarct
size elevated by I/R.

Conclusions

Pinocembrin showed a neuroprotective effects through antioxidant, anti-in?ammatory and
antiapoptotic mechanisms.