Protective effect of sodium propionate in Aβ1-42 -induced neurotoxicity and spinal cord trauma. (April 2020)

• Record Type: Journal Article
• Authors: Filippone, A.; Lanza, M.; Campolo, M.; Casili, G.; Paterniti, I.; Cuzzocrea, S.; Esposito, E.
• Is Part Of: Neuropharmacology. Volume 166(2020)
• Publication Date: 2020-04
• Subjects: Sodium propionate -- Short chain fatty acids -- Neuroprotection -- NF-κB -- Neuroinflammation -- Cytokines; Sodium propionate (SP) -- Short Chain Fatty Acids (SCFA) -- Amyloid beta 1-42 (Aβ1-42) -- Cicloxigenase-2 (COX-2) -- inducible nitric oxide synthase (iNOS) -- nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) -- Nitric Oxide (NO) -- Interleukin 1 6 (IL-6) -- Interleukin 8 (IL-8) -- Interleukin 1 beta (IL-1β) -- Tumor Necrosis Factor α (TNF-α) -- Histone deacetylase (HDAC) -- Eagle's Minimum Essential Medium (EMEM) -- Retinoic Acid (RA) -- dimethyl sulfoxide (DMSO) -- Central Nervous System (CNS) -- nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, α (IκBα) -- glial fibrillary acidic protein (GFAP) -- ionized calcium-binding adaptor protein-1 (Iba1) -- spinal cord injury (SCI) -- myeloperoxidase (MPO) -- malondialdehyde (MDA); Neuropsychopharmacology -- Periodicals; Autonomic Agents -- Periodicals; Neuropsychopharmacologie -- Périodiques; Neuropsychopharmacology; Periodicals; Electronic journals; 615.78
• DOI: 10.1016/j.neuropharm.2020.107977
• Languages: English
• ISSNs: 0028-3908

Abstract

Abstract: 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 mediators in an in vivo model of colitis. The aim of this study is to 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 Aβ1-42 stimulation, and in in vivo model of spinal cord injury (SCI) in which neuroinflammation plays a crucial role. For in vitro model, the human neuroblastoma SH-SY5Y cell line was first differentiated with retinoic acid (100 μM) for 24 h and then stimulated by oligomeric Aβ1-42 (1 μg/ml) and treated with SP at 0.1- 1–10 μM concentrations for another 24 h. 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 dose-dependent manner. In conclusion, our results demonstrated that SP possesses neuroprotective effects, suggesting it could represent a target for therapeutic intervention in neuroinflammatory disorders. Graphical abstract: Image 1 Highlights: SP is classified such as short chain fatty acid. SP possess anti-inflammatory effects. SP prevent Aβ 1-42 damage on mature neurons. SP restore damaged tissues after spinal cord injury. SP reducing pro-inflammatory mediators and cytokines.