Abstract
Berberis koreana extract (BE) has a strong neuroprotective effect after ischemic stroke in gerbils, which is associated with the inhibition of the N-methyl-d-aspartate receptor. The present study examined the antiinflammatory mechanism of BE after ischemic damage in vitro and in vivo. The BE used contained on average 7.39 +/- 0.78 mg/g of berberine. In PC12 cells with inflammation, prostaglandin E2 (PGE2) production was significantly reduced by BE. About 75% of pyramidal cells in the hippocampal CA1 region of gerbils exposed to 5 min of transient ischemia were protected from ischemic damage by BE. Cyclooxygenase-2 (COX-2) immunoreactivity and its protein level in the CA1 region of vehicle-treated animals exposed to an ischemic insult increased with time post-ischemia, whereas no such changes were observed in BE-treated animals exposed to ischemia. PGE2 production in BE-treated ischemic animals was significantly lower than that observed in vehicle-treated ischemic animals. Summarizing, the potent neuroprotective effect of BE was found to be due to the inhibitions of COX-2 expression and PGE2 production and its antiinflammatory activity.
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