decursin isolated from angelica gigas nakai rescues pc12 cells from amyloid β-protein-induced neurotoxicity through nrf2-mediated upregulation of heme oxygenase-1: potential roles of mapk
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2013
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Abstract
Decursin (D), purified from Angelica gigas Nakai, has been proven to exert neuroprotective property. Previous study revealed that D reduced Aβ25‒35-induced cytotoxicity in PC12 cells. Our study explored the underlying mechanisms by which D mediates its therapeutic effects in vitro. Pretreatment of cells with D diminished intracellular generation of ROS in response to Aβ25‒35. Western blot revealed that D significantly increased the expression and activity of HO-1, which was correlated with its protection against Aβ25‒35-induced injury. Addition of ZnPP, an HO-1 competitive inhibitor, significantly attenuated its protective effect in Aβ25‒35-treated cells, indicating the vital role of HO-1 resistance to oxidative injury. Moreover, D induced Nrf2 nuclear translocation, the upstream of HO-1 expression. While investigating the signaling pathways responsible for HO-1 induction, D activated ERK and dephosphorylated p38 in PC12 cells. Addition of U0126, a selective inhibitor of ERK, blocked D-induced Nrf2 activation and HO-1 induction and meanwhile reversed the protection of D against Aβ25‒35-induced cell death. These findings suggest D augments cellular antioxidant defense capacity through both intrinsic free radical scavenging activity and activation of MAPK signal pathways that leads to Nrf2 activation, and subsequently HO-1 induction, thereby protecting the PC12 cells from Aβ25‒35-induced oxidative cytotoxicity.
| Reference Key |
li2013evidence-baseddecursin
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|---|---|
| Authors | ;Li Li;Ji-kun Du;Li-yi Zou;Tie Wu;Yong-woo Lee;Yong-ho Kim |
| Journal | ACS applied materials & interfaces |
| Year | 2013 |
| DOI |
10.1155/2013/467245
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