Sulforaphane protects against rotenone-induced neurotoxicity in vivo: Involvement of the mTOR, Nrf2, and autophagy pathways
Zhou Q, Chen B, Wang X, Wu L, Yang Y, Cheng X, Hu Z, Cai X, Yang J, Sun X, Lu W, Yan H, Chen J, Ye J, Shen J, Cao P
Scientific reports · 128 citations
How it was studied
- Design
- Animal study (classified by our AI screen)
- Studied in
- Animals
- Main outcome
- Health markers and function
Who paid for it
- Funding
- Independent funding
- Government
- National Natural Science Foundation of China
- Government
- Government of Jiangsu Province
- Government
- Natural Science Foundation of Jiangsu Province
- Grants
- National Natural Science Foundation of China (81573964); Natural Science Foundation of Jiangsu Province (BK20161082); National Natural Science Foundation of China (81274150); Government of Jiangsu Province (BK20140049)
Based on 3 listed funder(s) and full-text disclosure statement.
Publication
- Published
- 2016-08-24 · Sci Rep · vol. 6 · issue 1 · p. 32206
- Publisher
- Nature Portfolio
- Cited
- 174 citations · more than 98% of similar papers · 7.5× the field average
- Impact
- Top 10% most cited in its field
- References
- 61 works
- Access
- Open access (journal) · CC-BY
- Research areas
- Genomics, phytochemicals, and oxidative stress · Calcium signaling and nucleotide metabolism · Autophagy in Disease and Therapy
- Keywords
- Sulforaphane, Rotenone, Neuroprotection, Glutathione, Neurotoxicity, Oxidative stress, Pharmacology, Chemistry, Autophagy, PI3K/AKT/mTOR pathway, Biochemistry, Biology, Apoptosis, Toxicity, Mitochondrion, Enzyme
- MeSH
- cell line, animals, mice, inbred balb c, humans, parkinson disease, neurotoxicity syndromes, disease models, animal, isothiocyanates, sulfoxides, rotenone, glutathione, neuroprotective agents, autophagy, male, nf-e2-related factor 2, tor serine-threonine kinases, dopaminergic neurons
16 authors
From CN
- Qian ZhouNanjing University of Chinese Medicine
- Bin Chen
- Xindong WangNanjing University of Chinese Medicine
- Lixin WuNanjing University of Chinese Medicine
- Yang YangNanjing University of Chinese Medicine; Jiangsu Provincial Academy of Traditional Chinese Medicine
- Xiaolan ChengNanjing University of Chinese Medicine; Jiangsu Provincial Academy of Traditional Chinese Medicine
Abstract
Sulforaphane, a naturally occurring compound found in cruciferous vegetables, has been shown to be neuroprotective in several neurological disorders. In this study, we sought to investigate the potential protective effects and associated molecular mechanisms of sulforaphane in an in vivo Parkinson's disease (PD) model, based on rotenone-mediated neurotoxicity. Our results showed that sulforaphane inhibited rotenone-induced locomotor activity deficiency and dopaminergic neuronal loss. Additionally, sulforaphane treatment inhibited the rotenone-induced reactive oxygen species production, malondialdehyde (MDA) accumulation, and resulted in an increased level of total glutathione and reduced glutathione (GSH): oxidized glutathione (GSSG) in the brain. Western blot analysis illustrated that sulforaphane increased the expression of nuclear factor (erythroid-derived 2)-like 2 (Nrf2), heme oxygenase-1 (HO-1), and NAD(P)H quinone oxidoreductase (NQO1), the latter two of which are anti-oxidative enzymes. Moreover, sulforaphane treatment significantly attenuated rotenone-inhibited mTOR-mediated p70S6K and 4E-BP1 signalling pathway, as well as neuronal apoptosis. In addition, sulforaphane rescued rotenone-inhibited autophagy, as detected by LC3-II. Collectively, these findings demonstrated that sulforaphane exert neuroprotective effect involving Nrf2-dependent reductions in oxidative stress, mTOR-dependent inhibition of neuronal apoptosis, and the restoration of normal autophagy. Sulforaphane appears to be a promising compound with neuroprotective properties that may play an important role in preventing PD.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY).
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