Mulberry Fruit Hot Water Extract Attenuates Adipose Tissue Inflammation with the Regulation of Macrophage Infiltration and M1/M2 Type Switching in Rats Fed a High-Fat Diet

Abstract

Abstract Objectives This study aimed to investigate the effects of mulberry fruit extract (ME) on adipose tissue inflammation in rats fed a high-fat diet. Methods Male, Sprague-Dawley rats were divided into 4 groups and fed either a low-fat diet (LF, 10% kcal fat), high-fat diet (HF, 45% kcal fat), HF with 0.5% mulberry fruit extract (HF + LME), or HF with 1% mulberry fruit extract (HF + HME) for 14 weeks. Results The serum triglyceride (TG) and total cholesterol (TC) concentrations were significantly lower in the ME supplemented groups. In white adipose tissue (WAT), the HF + HME significantly down-regulated the mRNA expression of adipogenic genes, such as sterol regulatory element-binding protein-1c (SREBP-1c), peroxisome proliferator-activated receptor-γ (PPAR-γ), and adipocyte protein2 (aP2). The HF + HME significantly decreased both levels of mRNA and protein of pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and monocyte chemoattractant protein 1 (MCP1). The crown-like structure (CLS) and the mRNA expression of F4/80, a pan-macrophage marker, tended to be reduced in the ME supplemented groups. The ME supplemented groups down-regulated the mRNA expression of pro-inflammatory M1 macrophage markers, such as a cluster of differentiation (CD) 68, CD11c, and nitric oxide synthase 2 (NOS2). On the other hand, the mRNA expression of CD163 and arginase1 (ARG1), an anti-inflammatory M2 macrophage marker, was up-regulated by the HF + HME. Conclusions From these results, it is suggested that the ME might modulate the macrophage infiltration and phenotypic switching and alleviate adipose tissue inflammation in rats fed a high-fat diet. Funding Sources None.