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 citas
Cómo se estudió
- Diseño
- Estudio en animales (clasificado por nuestro filtro de IA)
- Estudiado en
- Animales
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiación independiente
- Gobierno
- National Natural Science Foundation of China
- Gobierno
- Government of Jiangsu Province
- Gobierno
- Natural Science Foundation of Jiangsu Province
- Subvenciones
- 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)
Según 3 financiadores declarados y la declaración de financiación del texto completo.
Publicación
- Publicado
- 2016-08-24 · Sci Rep · vol. 6 · número 1 · pág. 32206
- Editorial
- Nature Portfolio
- Citado
- 174 citas · más que el 98% de estudios similares · 7.5× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 61 trabajos
- Acceso
- Acceso abierto (revista) · CC-BY
- Áreas de investigación
- Genomics, phytochemicals, and oxidative stress · Calcium signaling and nucleotide metabolism · Autophagy in Disease and Therapy
- Palabras clave
- 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 autores
- Qian Zhou🇨🇳Nanjing University of Chinese Medicine
- Bin Chen
- Xindong Wang🇨🇳Nanjing University of Chinese Medicine
- Lixin Wu🇨🇳Nanjing University of Chinese Medicine
- Yang Yang🇨🇳Nanjing University of Chinese Medicine; Jiangsu Provincial Academy of Traditional Chinese Medicine
- Xiaolan Cheng🇨🇳Nanjing University of Chinese Medicine; Jiangsu Provincial Academy of Traditional Chinese Medicine
- Zhengli Hu🇨🇳Nanjing University of Chinese Medicine
- Xueting Cai🇨🇳Nanjing University of Chinese Medicine; Jiangsu Provincial Academy of Traditional Chinese Medicine
- Jie Yang🇨🇳Nanjing University of Chinese Medicine; Jiangsu Provincial Academy of Traditional Chinese Medicine
- Xiaoyan Sun🇨🇳Nanjing University of Chinese Medicine; Jiangsu Provincial Academy of Traditional Chinese Medicine
- Wuguang Lu🇨🇳Nanjing University of Chinese Medicine; Jiangsu Provincial Academy of Traditional Chinese Medicine
- Huaijiang Yan🇨🇳Nanjing University of Chinese Medicine; Jiangsu Provincial Academy of Traditional Chinese Medicine
- Jiao Chen🇨🇳Nanjing University of Chinese Medicine; Jiangsu Provincial Academy of Traditional Chinese Medicine
- Juan Ye🇨🇳Nanjing University of Chinese Medicine; Jiangsu Provincial Academy of Traditional Chinese Medicine
- Jianping Shen🇨🇳Nanjing University of Chinese Medicine
- Peng Cao🇨🇳Nanjing University of Chinese Medicine; Jiangsu Provincial Academy of Traditional Chinese Medicine
Resumen
El texto original del estudio, en el idioma en que se publicó.
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.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY).
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