Neuroprotective effects of sulforaphane on methylglyoxal-induced glycation in SH-SY5Y cell line

Glycation, an endogenous process that leads to the production of advanced glycation end products (AGEs), plays a role in the etiopathogenesis of Alzheimer's disease (AD). Methylglyoxal (MG) is the most potent precursor of AGEs. It has been demonstrated that AGEs cause a reduction in brain derived neurotrophic factor protein (BDNF), whose dysregulation is related to AD development. Sulforaphane (SF), an isothiocyanate found in Cruciferous vegetables, is known for its chemopreventive, cardioprotective and neuroprotective actions. Aim of this study was to investigate the role of SF in counteracting MG induced damage in SH-SY5Y neuroblastoma cells. SF counteracted MG- induced neuronal death and apoptosis as measured by MTT assay, LDH release and caspase 3 activity. SF significantly reduced intracellular ROS and increased GSH levels in MG treated cells. SF inhibited the phosphorylation of the pro-apoptotic MAPK kinases induced by MG, increased the expression and the activity of the detoxifying glyoxalase enzymes GLO1 and GLO2 and increased BDNF expression of BDNF, demonstrating a pleiotropic role in counteracting AD. This work was supported by MIUR-FIRB (project RBAP11HSZS)