PMID- 27983705 OWN - NLM STAT- MEDLINE DCOM- 20170428 LR - 20200225 IS - 1420-3049 (Electronic) IS - 1420-3049 (Linking) VI - 21 IP - 12 DP - 2016 Dec 15 TI - Riboflavin Reduces Pro-Inflammatory Activation of Adipocyte-Macrophage Co-culture. Potential Application of Vitamin B2 Enrichment for Attenuation of Insulin Resistance and Metabolic Syndrome Development. LID - 1724 AB - Due to the progressive increase in the incidence of obese and overweight individuals, cardiometabolic syndrome has become a worldwide pandemic in recent years. Given the immunomodulatory properties of riboflavin, the current study was performed to investigate the potency of riboflavin in reducing obesity-related inflammation, which is the main cause of insulin resistance, diabetes mellitus 2 or arteriosclerosis. We determined whether pretreatment with a low dose of riboflavin (10.4-1000 nM) affected the pro-inflammatory activity of adipocyte-macrophage co-culture (3T3 L1-RAW 264.7) following lipopolysaccharide stimulation (LPS; 100 ng/mL) which mimics obesity-related inflammation. The apoptosis of adipocytes and macrophages as well as tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6), interleukin 1beta (IL-1beta), monocyte chemotactic protein 1 (MCP-1), high-mobility group box 1 (HMGB1), transforming growth factor-beta 1 (TGFbeta), interleukin 10 (IL-10), inducible nitric oxide synthase (iNOS), nitric oxide (NO), matrix metalloproteinase 9 (MMP-9), tissue inhibitor of metalloproteinases-1 (TIMP-1) expression and release, macrophage migration and adipokines (adiponectin and leptin) were determined. Our results indicated an efficient reduction in pro-inflammatory factors (TNFalpha, IL-6, MCP-1, HMGB1) upon culture with riboflavin supplementation (500-1000 nM), accompanied by elevation in anti-inflammatory adiponectin and IL-10. Moreover, macrophage migration was reduced by the attenuation of chemotactic MCP-1 release and degradation of the extracellular matrix by MMP-9. In conclusion, riboflavin effectively inhibits the pro-inflammatory activity of adipocyte and macrophage co-cultures, and therefore we can assume that its supplementation may reduce the likelihood of conditions associated with the mild inflammation linked to obesity. FAU - Mazur-Bialy, Agnieszka Irena AU - Mazur-Bialy AI AD - Department of Ergonomics and Exercise Physiology, Faculty of Health Science, Jagiellonian University Medical College, Grzegorzecka 20, 31-531 Krakow, Poland. agnieszka.mazur@uj.edu.pl. FAU - Pochec, Ewa AU - Pochec E AD - Department of Glycoconjugate Biochemistry, Institute of Zoology, Jagiellonian University, Gronostajowa 9, 30-387 Krakow, Poland. ewa.pochec@uj.edu.pl. LA - eng PT - Journal Article DEP - 20161215 PL - Switzerland TA - Molecules JT - Molecules (Basel, Switzerland) JID - 100964009 RN - 0 (Adiponectin) RN - 0 (Ccl2 protein, mouse) RN - 0 (Chemokine CCL2) RN - 0 (IL10 protein, mouse) RN - 0 (Lipopolysaccharides) RN - 130068-27-8 (Interleukin-10) RN - EC 3.4.24.35 (Matrix Metalloproteinase 9) RN - EC 3.4.24.35 (Mmp9 protein, mouse) RN - TLM2976OFR (Riboflavin) SB - IM MH - 3T3-L1 Cells MH - Adipocytes/cytology/immunology/*pathology MH - Adiponectin/metabolism MH - Animals MH - Apoptosis/*drug effects MH - Cell Line MH - Cell Movement/drug effects MH - Chemokine CCL2/metabolism MH - Coculture Techniques MH - Extracellular Matrix/metabolism MH - Inflammation/drug therapy/immunology MH - Insulin Resistance/physiology MH - Interleukin-10/metabolism MH - Lipopolysaccharides MH - Macrophages/cytology/immunology/*pathology MH - Matrix Metalloproteinase 9/metabolism MH - Metabolic Syndrome/drug therapy/*prevention & control MH - Mice MH - Obesity/*pathology MH - Riboflavin/*pharmacology PMC - PMC6273179 OTO - NOTNLM OT - adipocyte tissue OT - inflammation OT - insulin resistance OT - metabolic syndrome OT - obesity OT - obesity-related inflammation OT - riboflavin COIS- The authors declare no conflict of interest. EDAT- 2016/12/17 06:00 MHDA- 2017/04/30 06:00 PMCR- 2016/12/15 CRDT- 2016/12/17 06:00 PHST- 2016/11/01 00:00 [received] PHST- 2016/12/04 00:00 [revised] PHST- 2016/12/09 00:00 [accepted] PHST- 2016/12/17 06:00 [entrez] PHST- 2016/12/17 06:00 [pubmed] PHST- 2017/04/30 06:00 [medline] PHST- 2016/12/15 00:00 [pmc-release] AID - molecules21121724 [pii] AID - molecules-21-01724 [pii] AID - 10.3390/molecules21121724 [doi] PST - epublish SO - Molecules. 2016 Dec 15;21(12):1724. doi: 10.3390/molecules21121724.