Decursin attenuates the amyloid-beta-induced inflammatory response in PC12 cells via MAPK and nuclear factor-kappa B pathway

Abstract

Decursin, the major bioactive component of Angelica gigas Nakai, exhibited neuroprotective properties. Our previous studies showed that decursin conferred neuroprotective effects in PC12 cells induced by Amyloid-beta (A beta)(25-35) via antiapoptosis and antioxidant. In this study, the antiinflammatory effects of decursin against PC12 cells injury stimulated by A beta(25-35) were assessed. Our results demonstrated that decursin suppressed the expression of cyclooxygenase-2 protein and prostaglandin E2 content which was stimulated by A beta(25-35) in PC12 cells. Meanwhile, the nuclear translocation of nuclear factor-kappa B in A beta(25-35)-treated PC12 cells was also inhibited by decursin. In addition, decursin suppressed phosphorylation of the two upstream pathway kinases, p38 and c-Jun N-terminal kinase. Overall, our findings indicate that decursin exerts protective effects against neuroinflammation stimulated by A beta(25-35) in PC12 cells by abolishing cyclooxygenase-2 protein expression through inactivation of nuclear factor-kappa B via the upstream kinases including p38 and c-Jun N-terminal kinase. This work provides a new insight into the pharmacological mode of decursin and should facilitate its therapeutic application in treatment of inflammatory disorders.