Abstract Title:

Puerarin attenuates neuronal degeneration in the substantia nigra of 6-OHDA-lesioned rats through regulating BDNF expression and activating the Nrf2/ARE signaling pathway.

Abstract Source:

Brain Res. 2013 Jul 26 ;1523:1-9. Epub 2013 Jun 5. PMID: 23747813

Abstract Author(s):

Rong Li, Tao Liang, Lingyuan Xu, Ni Zheng, Kefeng Zhang, Xiaoqun Duan

Article Affiliation:

Rong Li


An increasing number of studies suggest that oxidative stress is associated with the Parkinsonian process. This study evaluated the potential neuroprotective role of puerarin (PR) on lesioned substantia nigra (SN) induced by 6-hydroxydopamine (6-OHDA). Data from a rotational test showed that PR treatment significantly decreased apomorphine-induced rotations. Both the dopamine (DA) content in the SN and the endogenous expression of brain-derived neurotrophic factor (BDNF) were also elevated by the treatment. Pathological examination showed that dopaminergic neuronal degeneration in the SN was attenuated by PR treatment. Meanwhile, the contents ofγ-glutamylcysteine synthetase (γ-GCS), glutathione (GSH) and catalase (CAT) in SN tissue were gradually elevated. Additionally, cytochrome c oxidase (COX) mRNA expression in the SN was markedly up-regulated. At the same time, nuclear factor E2-related factor 2 (Nrf2) and Kelch-like ECH-associatedprotein 1 (Keapl) levels were progressively increased by the PR treatment. Our findings indicated that puerarin effectively protects against 6-OHDA-mediated oxidative stress injury in SN neurons, in which the underlying mechanisms are involved in modulating BDNF expression and activating the Nrf2/ARE signaling pathway.

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