The Effects of Chrysanthemum morifolium Flower Extract on Obesity-Induced Inflammation and Muscle AMPK/SIRT1 Activities in Obese Rats

Abstract Objectives The objective of this study is to investigate the effects of hot water extract of Chrysanthemum morifolium Ramat flower (CE) on obesity-induced inflammation and skeletal muscle mitochondrial function in high-fat diet fed rats. Methods Male Sprague-Dawley rats (3-week-old) were randomly divided into 4 groups, and fed with a normal diet (NOR), high fat diet (HF), HF containing 0.2% CE (CEL) or 0.4% CE (CEH) for 13 weeks. Results CE reduced body weight and total white adipose tissue weights. The levels of serum triglyceride (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) significantly reduced in the CEL and CEH groups compared to the HF group. In white adipose tissue, CE attenuated HF-induced adipose tissue macrophage (ATM) infiltration and down-regulated F4/80 mRNA expression compared to the HF group. In addition, CE down-regulated the mRNA levels involved in inflammation and ATM polarization, such as tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), monocyte chemoattracted protein-1 (MCP1), inducible nitric oxide synthase (iNOS), and cluster of differentiation 11c (CD11c) compared to the HF group. On the other hand, gene expression of arginase 1 (Arg1), a M2 macrophage marker was significantly up-regulated in the CEL and CEH groups compared to the HF group. Nuclear factor-kappa B (NF-κB) activities and serum nitric oxide (NO) concentrations were significantly decreased by CE supplementation. In skeletal muscle, mitochondrial size and mitochondrial DNA (mtDNA) content were significantly increased in the CEL and CEH groups compared to the HF group. CE supplementation were also up-regulated the mRNA expression related to mitochondrial function, including sirtuin 1 (SIRT1), peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), and carnitine palmitoyltransferase 1β (CPT-1β). Furthermore, activities of AMP-activated protein kinase (AMPK) and SIRT1 were increased by CE supplementation. Conclusions These results suggested that CE attenuates obesity-induced inflammation via regulating M1/M2 macrophage and increases the muscle mitochondria content and AMPK/SIRT1 activities. Funding Sources This research was supported by the BK21 FOUR (Fostering Outstanding Universities for Research) funded by the Ministry of Education (MOE, Korea) and National Research Foundation of Korea (NRF).