Ameliorative Effect of Raspberry Ketone on Hypothalamic Inflammation in High Fat Diet-Induced Obese Mice

Abstract

This study aimed to investigate the regulatory effects of raspberry ketone on hypothalamic inflammation and its mechanism. Mouse microglia cells (BV2 cells) were cultured in vitro with palmitic acid (100 μM) to induce inflammation model and then incubated with raspberry ketone (5, 20, 50 μM) alone or raspberry ketone (50 μM) and the specific inhibitor of uncoupling protein 2 (UCP2), genipin (10 μM), to test the role of UCP2 in raspberry ketone regulatory of inflammation. Meanwhile, C57BL/6J mice were fed a high-fat diet containing raspberry ketone (0.2%, wt/wt) for 16 wk or 7 d to observe the effects of raspberry ketone on the body weights and hypothalamic inflammation of mice. The expression levels of inflammatory factors, including interleukin-6 (IL-6), interleukin-1beta (IL-1β) and tumour necrosis factor alpha (TNF-α), were detected using RT-qPCR, Elisa, and Western blotting, respectively. At the cellular level, raspberry ketone reduced the content of inflammatory factors in BV2 cells and in the cell culture medium. Genipin inhibited the anti-inflammatory effect of raspberry ketone on BV2 cells. At the animal level, after 16 wk of feeding, raspberry ketone-containing diets significantly reduced the body weight of mice, but had no significant effect on the mRNA expression level of hypothalamic inflammatory factors. On the other hand, 7 d of raspberry ketone gavage significantly reduced mRNA and protein expression of hypothalamic inflammatory factors. The results of this study suggest that raspberry ketone could regulate high-fat diet-induced obesity in mice, and the specific mechanism may be to inhibit hypothalamic inflammation in mice by regulating UCP2 gene expression.