Abstract
Background: Tissue type 2 transglutaminase (TG2, E.C. 2.3.2,13) is reported to be involved in the phagocytosis of apoptotic cells in mouse microglial BV2 cells and peripheral macrophages. In this study, by using lipopolysaccharide (LPS)- or amyloid-β 1-42 (Aβ 1-42) peptide-stimulated microglial 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 biomarker expressions. Methods: Mouse BV2 cells were treated with LPS or Aβ1-42 in the presence of curcumin or PEA, in order to evaluate the expression of TG2 and other inflammatory or neuroprotective markers using Real Time-PCR and Western blot analyses. Results: Curcumin and PEA were capable of reducing TG2 expression in mouse microglial cells during co-treatment with LPS or Aβ 1-42. Conclusions: The results show the role of TG2 as an important marker of neuroinflammation and suggest a possible use of curcumin and PEA in order to reduce LPS- or Aβ1-42-induced TG2 overexpression in mouse microglial cells.
Highlights
Transglutaminases (TGs; EC 2.3.2.13) are a family of calcium-dependent enzymes that catalyze the cross-linking of proteins by promoting the formation of isopeptide bonds between protein-bound glutamine and lysine residues
The data from numerous studies have demonstrated the involvement of TG2 in Celiac disease (CD), while more recently, a large body of literature has suggested that TG2 could be involved in neurodegenerative disorders, including Alzheimer’s disease (AD), Parkinson’s disease (PD) and other neurodegenerative diseases [18,19]
We initially focused the attention on the anti-inflammatory effects of PEA and curcumin, nutraceuticals tested under in vitro neuroinflammatory conditions induced by challenge with LPS
Summary
Transglutaminases (TGs; EC 2.3.2.13) are a family of calcium-dependent enzymes that catalyze the cross-linking of proteins by promoting the formation of isopeptide bonds between protein-bound glutamine and lysine residues. These enzymes are capable of catalyzed reactions, such as the attachment of a mono(poly)-amine to the γ-carboxamide of a glutaminyl residue and the deamidation of the γ-carboxamide group of a protein/polypeptide glutaminyl residue (for a review see [1,2]). By using lipopolysaccharide (LPS)- or amyloid-β 1-42 (Aβ 1-42) peptide-stimulated microglial 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 biomarker expressions. Results: Curcumin and PEA were capable of reducing TG2 expression in mouse microglial cells during co-treatment with LPS or Aβ 1-42
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