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A novel modified-curcumin 2.24 resolves inflammation by promoting M2 macrophage polarization.
- Source :
- Scientific Reports; 9/19/2023, Vol. 13 Issue 1, p1-14, 14p
- Publication Year :
- 2023
-
Abstract
- To assess resolving-like activity by a novel chemically-modified curcumin (CMC2.24) in a "two-hit" model of diabetes-associated periodontitis. Macrophages from rats were cultured in the presence/absence of either Lipopolysaccharide (LPS, 1st hit); or advanced-glycation-end products (AGE, 2nd hit); or both combined. CMC2.24 was added as treatment. The conditioned media were analyzed for MMP-9, cytokines (IL-1β, IL-6, TNF-α), resolvins (RvD<subscript>1</subscript>, RvE<subscript>1</subscript>, lipoxin A<subscript>4</subscript>), and soluble receptor for AGE (sRAGE). The phenotypes of M1/M2 macrophage were analyzed by flow cytometry. Both LPS/AGE-alone, and two-combined, dramatically increased the secretion of MMP-9 by macrophages. CMC2.24 "normalized" the elevated levels of MMP-9 under all conditions. Moreover, CMC2.24 significantly reduced the secretion of IL-1β and IL-6 with a fewer effects on TNF-α. Importantly, CMC2.24 increased RvD<subscript>1</subscript> and sRAGE secretion by macrophages exposed to LPS/AGE; and both treatment groups exhibited increased M2 relative to M1 populations. Furthermore, scatter-diagram showed the macrophages gradually shifted from M1 towards M2 with CMC2.24-treated, whereas LPS/AGE-alone groups remained unchanged. CMC2.24 "normalized" cytokines and MMP-9, but also enhanced RvD<subscript>1</subscript> and sRAGE in macrophages. Crucially, CMC2.24 appears to be a potent inhibitor of the pro-inflammatory M1 phenotype; and a promotor of the pro-resolving M2 phenotype, thus acting like a crucial "switch" to reduce inflammation. [ABSTRACT FROM AUTHOR]
- Subjects :
- MACROPHAGES
MATRIX metalloproteinases
FLOW cytometry
INFLAMMATION
INTERLEUKIN-6
Subjects
Details
- Language :
- English
- ISSN :
- 20452322
- Volume :
- 13
- Issue :
- 1
- Database :
- Complementary Index
- Journal :
- Scientific Reports
- Publication Type :
- Academic Journal
- Accession number :
- 172020014
- Full Text :
- https://doi.org/10.1038/s41598-023-42848-x