Sulforaphane reduces adipose tissue fibrosis via promoting M2 macrophages polarization in HFD fed-mice

Abstract Background/Objectives: Adipose tissue fibrosis has been identified as a novel contributor to the pathomechanism of obesity associated metabolic disorders. Sulforaphane (SFN) has been shown to have an anti-obesity effect. However, the impact of SFN on adipose tissue fibrosis is still not well understood. Methods: In this study, obese mice induced by high-fat diets (HFD) were used, and SFN was administered through subcutaneous injection to examined the effects on adipose tissue fibrosis. Analysis included quantification of: (i) body weight, food intake, fat mass, glucose tolerance and insulin tolerance; (ii) the relative mRNA and protein levels of fibrosis, inflammation and macrophages polarization related genes; (iii) tissue histology using Hematoxylin-Eosin (H&E), immunohistochemistry and immunofluorescent staining; and (iv) the levels of inflammatory cytokinesin serum. Results: According to the current findings, SFN dramatically enhanced glucose tolerance and decreased body weight in diet-induced-obesity (DIO) mice. Additionally, SFN therapy significantly reduced extracellular matrix (ECM) deposition and altered the expression of genes related to fibrosis. Furthermore, SFN also reduced inflammation and promoted macrophages polarization towards to M2 phenotype in adipose tissue, which protected adipose tissue from fibrosis. Notably, SFN-mediated nuclear factor E2-related factor 2 (Nrf2) activation was crucial in decreasing adipose tissue fibrosis. Conclusions: These results implied that SFN had favorable benefits in the management of adipose tissue fibrosis, which consequently ameliorates obesity-related metabolic problems. Our research provides new treatment strategies for obesity.