Chronic low-grade inflammation is a hallmark of obesity and its related metabolic disorders. At the same time signaling from pro-inflammatory factors such as transforming growth factor beta (TGF-β) or interleukin 17A (IL-17A) are proposed as crucial for the commitment of fibroblast progenitor cells towards adipogenic differentiation. Modulation of inflammation during adipogenic differentiation is incompletely explored as a potential approach to prevent metabolic disorders. Rosmarinic acid (RA) is a caffeic acid derivative known for its anti-inflammatory effects. Experimental studies of its activity on adipogenic factors or in vivo obesity models are, however, controversial and hence insufficient. Here, we investigated the anti-adipogenic action of RA in human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes. Gene expression levels of key players in adipogenesis and lipid metabolism were assessed. Furthermore, a molecular mechanism of action was proposed. The most prominent effect was found on the translation of C/EBPα, PPARγ and adiponectin, as well as on the modulation of TGF1B and IL17A. Interestingly, involvement of NRF2 signaling was identified upon RA treatment. In summary, our findings indicate that RA prevents inflammation and excessive lipid accumulation in human adipocytes. Data from the molecular analysis demonstrate that RA has potential for treatment of obesity and obesity-related inflammation.
Keywords: Adipocytes; Anti-Adipogenic action; Inflammation; Obesity; Orlistat (PubChem CID: 3034010); Rosmarinic acid; Rosmarinic acid (PubChem CID: 5281792).
Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.