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KMID : 0043320090320010109
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Archives of Pharmacal Research
2009 Volume.32 No. 1 p.109 ~ p.115
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Protection against Amyloid Beta Cytotoxicity by Sulforaphane: Role of the Proteasome
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Kwak Mi-Kyoung
Kim Jung-Ae
Park Hyun-Min
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Abstract
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The 26S proteasome plays a major role in degradation of abnormal proteins within the cell. The indirect antioxidant including sulforaphane (SFN) protects cells from oxidative damage by increasing the expression of Nrf2-target genes. It has been observed that the expression of multiple subunits of the proteasome was up-regulated by indirect antioxidants through the Nrf2 pathway. In the current study, the role of SFN in amyloid β1-42 (Aβ1-42)-induced cytotoxicity has been investigated in murine neuroblastoma cells. Treatment with SFN protected cells from Aβ1-42-mediated cell death in Neuro2A and N1E 115 cells. Inhibition of proteasome activities by MG132 could abolish the protective effect of SFN against Aβ1-42. Neuro2A cells, which were stably overexpressing the catalytic subunit of the proteasome PSMB5, showed an elevated resistance toward Aβ1-42 toxicity compared to control cells. Furthermore, the in vitro assay demonstrated that the Aβ1-42 peptide is degraded by the proteasome fraction. These results suggest that proteasome-inducing indirect antioxidants may facilitate the removal of the Aβ1-42 peptide and lead to the amelioration of abnormal protein-associated etiologies.
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KEYWORD
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26S proteasome, Indirect antioxidant, Sulforaphane, Amyloid beta, Protein aggregation
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