Neuroprotective effect of sulforaphane against methylglyoxal cytotoxicity
Angeloni C, Malaguti M, Rizzo B, Barbalace MC, Fabbri D, Hrelia S
Chemical research in toxicology · 82 citas
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- Estudio in vitro o de mecanismos (clasificado por nuestro filtro de IA)
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- Células o muestras de laboratorio
- Resultado principal
- Solo mecanismos
Quién lo pagó
- Financiación
- Financiación independiente
- Gobierno
- Ministero dell'Istruzione, dell'Università e della Ricerca
Según 1 financiador declarado.
Publicación
- Publicado
- 2015-05-01 · Chem Res Toxicol · vol. 28 · número 6 · págs. 1234–1245
- Editorial
- American Chemical Society
- Citado
- 92 citas · más que el 93% de estudios similares · 3.4× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 95 trabajos
- Acceso
- Acceso abierto (copia en repositorio) · OTHER-OA
- Áreas de investigación
- Genomics, phytochemicals, and oxidative stress · Biochemical Acid Research Studies · Nuclear Receptors and Signaling
- Palabras clave
- Sulforaphane, Methylglyoxal, Cytotoxicity, Neuroprotection, Chemistry, Pharmacology, Biochemistry, Medicine, In vitro
- MeSH
- tumor cells, cultured, humans, pyruvaldehyde, isothiocyanates, sulfoxides, glucose, neuroprotective agents, apoptosis, structure-activity relationship, oxidative stress, dose-response relationship, drug
6 autores
- Cristina Angeloni🇮🇹 · autor de correspondenciaUniversity of Bologna
- Marco Malaguti🇮🇹University of Bologna
- Benedetta Rizzo🇮🇹University of Bologna
- Maria Cristina Barbalace🇮🇹University of Bologna
- Daniele Fabbri🇮🇹University of Bologna
- Silvana Hrelia🇮🇹University of Bologna
Resumen
El texto original del estudio, en el idioma en que se publicó.
Glycation, an endogenous process that leads to the production of advanced glycation end products (AGEs), plays a role in the etiopathogenesis of different neurodegenerative diseases, such as Alzheimer's disease (AD). Methylglyoxal is the most potent precursor of AGEs, and high levels of methylglyoxal have been found in the cerebrospinal fluid of AD patients. Methylglyoxal may contribute to AD both inducing extensive protein cross-linking and mediating oxidative stress. The aim of this study was to investigate the role of sulforaphane, an isothiocyanate found in cruciferous vegetables, in counteracting methylglyoxal-induced damage in SH-SY5Y neuroblastoma cells. The data demonstrated that sulforaphane protects cells against glycative damage by inhibiting activation of the caspase-3 enzyme, reducing the phosphorylation of MAPK signaling pathways (ERK1/2, JNK, and p38), reducing oxidative stress, and increasing intracellular glutathione levels. For the first time, we demonstrate that sulforaphane enhances the methylglyoxal detoxifying system, increasing the expression and activity of glyoxalase 1. Sulforaphane modulated brain-derived neurotrophic factor and its pathway, whose dysregulation is related to AD development. Moreover, sulforaphane was able to revert the reduction of glucose uptake caused by methylglyoxal. In conclusion, sulforaphane demonstrates pleiotropic behavior thanks to its ability to act on different cellular targets, suggesting a potential role in preventing/counteracting multifactorial neurodegenerative diseases such as Alzheimer's.
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