Neuronutraceuticals Modulate Lipopolysaccharide- or Amyloid-β 1-42 Peptide-Induced Transglutaminase 2 Overexpression as a Marker of Neuroinflammation in Mouse Microglial Cells

Background: Tissue type 2 Transglutaminase (TG2, E.C. 2.3.2,13) is reported to be involved in phagocytosis of apoptotic cells in mouse microglial BV2 cells and peripheral macrophages. In this study, by using Lipopolysaccharide (LPS)- or Amyloid-beta 1-42 (Abeta 1-42) peptide-stimulated mi-croglial cell line BV2 and mouse primary microglial cells, we examined the effects of different neuronutraceutical compounds, such as Curcumin (Cu) and N-Palmitoylethanolamine (PEA), known for their anti-inflammatory activity, on TG2 and several inflammatory or neuroprotective biomarkers expressions. Methods: Mouse BV2 cells were treated with LPS or Abeta1-42 in presence of Curcumin or PEA, in order to evaluate the expression of TG2 and other inflammatory or neuro-protective markers by RealTime PCR and Western Blot analyses. Results: Curcumin and PEA were capable to reduce TG2 expression in mouse microglial cells during co-treatment with LPS or Abeta 1-42. Conclusions: The results show the role of TG2 as an important marker of neuroinflamma-tion and suggest a possible use of Curcumin and PEA, in order to reduce LPS- or Abeta1-42-induced TG2 overexpression in mouse microglial cells.