Decursin attenuates the amyloid‐β‐induced inflammatory response in PC12 cells via MAPK and nuclear factor‐κB pathway |
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Authors: | Li Li Yiqiu Yang Jingbin Zheng Guodi Cai Yongwoo Lee Jikun Du |
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Affiliation: | 1. Dongguan Scientific Research Center, Guangdong Medical University, Dongguan, China;2. Department of Smart Food and Drugs, Graduate School, Inje University, Gimhae, Republic of Korea;3. Department of Chemical and Biomolecular Engineering, Korea Advanced Institute of Science and Technology, Daejeon, Republic of Korea |
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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‐β (Aβ)25–35 via antiapoptosis and antioxidant. In this study, the antiinflammatory effects of decursin against PC12 cells injury stimulated by Aβ25–35 were assessed. Our results demonstrated that decursin suppressed the expression of cyclooxygenase‐2 protein and prostaglandin E2 content which was stimulated by Aβ25–35 in PC12 cells. Meanwhile, the nuclear translocation of nuclear factor‐κB in Aβ25–35‐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 Aβ25–35 in PC12 cells by abolishing cyclooxygenase‐2 protein expression through inactivation of nuclear factor‐κB 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. |
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Keywords: | amyloid– β decursin inflammatory MAPK nuclear factor– κ B |
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