Neuroprotective effect of sulforaphane against methylglyoxal cytotoxicity
Angeloni C, Malaguti M, Rizzo B, Barbalace MC, Fabbri D, Hrelia S
Chemical research in toxicology · 82 citations
Review labels
Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.
How it was studied
- Design
- In vitro/mechanistic study (classified by our AI screen)
- Studied in
- Cells or lab samples
- Main outcome
- Mechanisms only
Who paid for it
- Funding
- Independent funding
- Government
- Ministero dell'Istruzione, dell'Università e della Ricerca
Based on 1 listed funder(s).
Publication
- Published
- 2015-05-01 · Chem Res Toxicol · vol. 28 · issue 6 · pp. 1234–1245
- Publisher
- American Chemical Society
- Cited
- 92 citations · more than 93% of similar papers · 3.4× the field average
- Impact
- Top 10% most cited in its field
- References
- 95 works
- Access
- Open access (repository copy) · OTHER-OA
- Research areas
- Genomics, phytochemicals, and oxidative stress · Biochemical Acid Research Studies · Nuclear Receptors and Signaling
- Keywords
- 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 authors
From IT
- Cristina Angeloni · correspondingUniversity of Bologna
- Marco MalagutiUniversity of Bologna
- Benedetta RizzoUniversity of Bologna
- Maria Cristina BarbalaceUniversity of Bologna
- Daniele FabbriUniversity of Bologna
- Silvana HreliaUniversity of Bologna
Abstract
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.
Abstract via Europe PMC. Copyright remains with the authors or publisher.
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