Journal of Translational Neurosciences

Protective effect of Sodium propionate in Aβ1-42 -Induced Neurotoxicity and Spinal Cord Trauma

Sodium propionate (SP) is one of the main short chain fatty acids (SCFA) that can be produced naturally through host metabolic pathways. SP have been documented and include the reduction of pro-inflammatory mediatorsin an in vivo model of colitis. The aim of thisstudy isto evaluate the neuroprotective effects of SP in reducing inflammatory process associated to neurological disorders. We performed both in vitro model of Alzheimer’s disease, induced by oligomeric Abeta1-42 stimulation, and in in vivo model of spinal cord injury (SCI) in which neuroinflammation plays a crucialrole. Forin vitro model,the human neuroblastoma SH-SY5Y cell line wasfirst differentiated with retinoic acid (100 μM) for 24 hours and then stimulated by oligomeric Abeta1-42 (1μg/ml) and treated with SP at 0.1- 1- 10 μM concentrations for another 24 hours. Instead, the in vivo model of SCI was induced by extradural compression of the spinal cord at T6-T8 levels, and animals were treated with SP (10-30-100 mg/kg o.s) 1 and 6 h after SCI. Our results demonstrated that both in in vitro neuroinflammatory model and in vivo model of SCI the treatment with SP significantly reduced NF-κB nuclear translocation and IκBα degradation, as well as decreases COX-2 and iNOS expressions evaluated by Western blot analysis. Moreover, we showed that SP treatment significantly ameliorated histopathology changes and improved motor recovery in a dosedependent manner. In conclusion, our results demonstrated that SP possesses neuroprotective effects, suggesting it could represent a target for therapeutic intervention in neuroinflammatory disorders.

Irene Paterniti, Campolo Michela, Casili Giovanna, Lanza Marika, Filippone Alessia and Cuzzocrea Salvatore