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: 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 of γ-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-associated protein 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.
authors.affiliation: Guilin Medical University, Guilin, Guangxi 541004, PR China.
authors.forename: Rong
authors.initials: R
authors.lastname: Li
authors.forename: Tao
authors.initials: T
authors.lastname: Liang
authors.forename: Lingyuan
authors.initials: L
authors.lastname: Xu
authors.forename: Ni
authors.initials: N
authors.lastname: Zheng
authors.forename: Kefeng
authors.initials: K
authors.lastname: Zhang
authors.forename: Xiaoqun
authors.initials: X
authors.lastname: Duan
mesh_terms: D000818:Animals; D008297:Male; D051381:Rats; D000975:Antioxidants / Q000009:adverse effects / Q000494:pharmacology; D015153:Blotting, Western; D019208:Brain-Derived Neurotrophic Factor / Q000096:biosynthesis; D002374:Catalase / Q000378:metabolism; D004298:Dopamine / Q000378:metabolism; D003576:Electron Transport Complex IV / Q000378:metabolism; D005721:Glutamate-Cysteine Ligase / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D006892:Hydroxydopamines; D007150:Immunohistochemistry; D047908:Intracellular Signaling Peptides and Proteins / Q000096:biosynthesis / Q000235:genetics; D007529:Isoflavones / Q000009:adverse effects / Q000494:pharmacology; D000072019:Kelch-Like ECH-Associated Protein 1; D009410:Nerve Degeneration / Q000517:prevention & control; D018696:Neuroprotective Agents; D017208:Rats, Wistar; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology; D013378:Substantia Nigra / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D013565:Sympatholytics; D051267:NF-E2-Related Factor 2 / Q000096:biosynthesis
chemical_list: D000975:Antioxidants; D019208:Brain-Derived Neurotrophic Factor; D002374:Catalase; D004298:Dopamine; D003576:Electron Transport Complex IV; D005721:Glutamate-Cysteine Ligase; D005978:Glutathione; D006892:Hydroxydopamines; D047908:Intracellular Signaling Peptides and Proteins; D007529:Isoflavones; C486610:KEAP1 protein, rat; D000072019:Kelch-Like ECH-Associated Protein 1; D018696:Neuroprotective Agents; C033607:puerarin; D013565:Sympatholytics; D051267:NF-E2-Related Factor 2
keywords: BDNF; Nrf2/ARE signaling pathway; Oxidative stress; Parkinson's disease; Puerarin; Substantia nigra