Opuntia ficus-indica seed attenuates hepatic steatosis and promotes M2 macrophage polarization in high-fat diet-fed mice

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• 作者：Jung-Woo Kang^a ; Jun-Kyu Shin^a ; Eun-Ji Koh^b ; Hyojeong Ryu^b ; Hyoung Ja Kim^c ; Sun-Mee Lee^a ; ^{sunmee@skku.edu" class="auth_mail" title="E-mail the corresponding author}
• 关键词：High-fat diet fed mice ; Lipid accumulation ; Macrophage polarization ; Non-alcoholic fatty liver disease ; Opuntia ficus-indica seed ; Toll-like receptor 4
• 刊名：Nutrition Research
• 出版年：2016
• 出版时间：April 2016
• 年：2016
• 卷：36
• 期：4
• 页码：369-379
• 全文大小：958 K

文摘

Opuntia ficus-indica (L.) is a popular edible plant that possesses considerable nutritional value and exhibits diverse biological actions including anti-inflammatory and antidiabetic activities. In this study, we hypothesized that DWJ504, an extract of O ficus-indica seed, would ameliorate hepatic steatosis and inflammation by regulating hepatic de novo lipogenesis and macrophage polarization against experimental nonalcoholic steatohepatitis. Mice were fed a normal diet or a high-fat diet (HFD) for 10 weeks. DWJ504 (250, 500, and 1000 mg/kg) or vehicle (0.5% carboxymethyl cellulose) were orally administered for the last 4 weeks of the 10-week HFD feeding period. DWJ504 treatment remarkably attenuated HFD-induced increases in hepatic lipid content and hepatocellular damage. DWJ504 attenuated increases in sterol regulatory element-binding protein 1 and carbohydrate-responsive element-binding protein expression and a decrease in carnitine palmitoyltransferase 1A. Although DWJ504 augmented peroxisome proliferator–activated receptor α protein expression, it attenuated peroxisome proliferator–activated receptor γ expression. Moreover, DWJ504 promoted hepatic M2 macrophage polarization as indicated by attenuation of the M1 marker genes and enhancement of M2 marker genes. Finally, DWJ504 attenuated expression of toll-like receptor 4, nuclear factor κB, tumor necrosis factor α, interleukin 6, TIR-domain-containing adapter–inducing interferon β, and interferon β levels. Our results demonstrate that DWJ504 prevented intrahepatic lipid accumulation, induced M2 macrophage polarization, and suppressed the toll-like receptor 4–mediated inflammatory signaling pathway. Thus, DWJ504 has therapeutic potential in the prevention of nonalcoholic fatty liver disease.