Activation of Nrf2 signaling by Icariin protects against 6-OHDA-induced neurotoxicity.
In: Biotechnology and applied biochemistry, Jg. 66 (2019-05-01), Heft 3, S. 465-471
Online
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Zugriff:
Nerve damage is the main pathogenesis of neurodegenerative diseases. Recently, in search for a promising therapeutic target that could stop neurodegenerative diseases progression, the antioxidant signaling pathway regulated by transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) has attracted new hopes. Icariin (ICA) exhibited a battery of pharmacological properties, including antioxidation, anti-aging, and anti-inflammation activities. Recent studies indicate ICA conferred neuroprotection against brain ischemic injury and neurodegenerative diseases. However, the mechanisms underlying ICA-mediated neuroprotection remain unelucidated. This study aimed at analyzing whether ICA evoked neuroprotection against 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in PC12 cells and the mechanisms of action. ICA protected against 6-OHDA-induced neuronal damage, accompanied by the inhibition of cell apoptosis through the marked decreases in the Bax/Bcl-2 ratio, cytochrome c release, and caspase-3 cleavage. In addition, the activation of Nrf2 signaling pathway was responsible for ICA-mediated neuroprotection. First, ICA relieved reactive oxygen species accumulation and increased superoxide dismutase generation via the activation of Nrf2 signaling. Second, Nrf2 knockdown by siRNA reversed ICA-mediated neuroprotection. Together, these results suggested ICA-mediated neuroprotection might be attributable to the activation of Nrf2 pathway via antioxidative signaling pathways.
(© 2019 International Union of Biochemistry and Molecular Biology, Inc.)
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Activation of Nrf2 signaling by Icariin protects against 6-OHDA-induced neurotoxicity.
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Autor/in / Beteiligte Person: | Zhu, L ; Li, D ; Chen, C ; Wang, G ; Shi, J ; Zhang, F |
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Zeitschrift: | Biotechnology and applied biochemistry, Jg. 66 (2019-05-01), Heft 3, S. 465-471 |
Veröffentlichung: | Jan. 2011- : Malden : Wiley-Blackwell ; <i>Original Publication</i>: San Diego : Academic Press, [cl986]-, 2019 |
Medientyp: | academicJournal |
ISSN: | 1470-8744 (electronic) |
DOI: | 10.1002/bab.1743 |
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