Activation of Nrf2 signaling by Icariin protects against 6-OHDA-induced neurotoxicity.
Biotechnol Appl Biochem
; 66(3): 465-471, 2019 May.
Article
em En
| MEDLINE
| ID: mdl-30892727
ABSTRACT
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.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Flavonoides
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Medicamentos de Ervas Chinesas
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Transdução de Sinais
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Oxidopamina
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Fármacos Neuroprotetores
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Fator 2 Relacionado a NF-E2
Limite:
Animals
Idioma:
En
Revista:
Biotechnol Appl Biochem
Assunto da revista:
BIOQUIMICA
/
BIOTECNOLOGIA
Ano de publicação:
2019
Tipo de documento:
Article