Cerasus humilis Cherry Polyphenol Reduces High-Fat Diet-Induced Obesity in C57BL/6 Mice by Mitigating Fat Deposition, Inflammation, and Oxidation
Cerasus humilis Cherry Polyphenol Reduces High-Fat Diet-Induced Obesity in C57BL/6 Mice by Mitigating Fat Deposition, Inflammation, and Oxidation
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DOI：
10.1021/acs.jafc.0c01617
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发表时间：
2020-04-15
影响因子：
6.1
通讯作者：
Xu, Weifeng
中科院分区：
文献类型：
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作者：
Liu, Suwen;Chang, Xuedong;Xu, Weifeng
本研究旨在探讨矮樱桃多酚（CHP）对CS 7 BL/6肥胖小鼠和3 T3-L1细胞的减肥作用及其机制。采用高效液相色谱-电喷雾串联质谱法对CHP组分进行定性和定量鉴定。采用高脂饲料（HFD）诱导的肥胖小鼠，灌胃给予CHP（250 mg/kg/d）12周。以15.6 mg/kg bw/天的剂量灌胃奥利司他，作为阳性对照组。结果表明，CHP的主要成分为原花青素B2、矢车菊素-3-葡萄糖苷和天竺葵素-3-葡萄糖苷。CHP膳食补充显著降低了HFD喂养小鼠的体重并改善了血脂测量（p < 0.01）。此外，它抑制miR-122、Srebp-lc和Cpt 1a的mRNA表达（p < 0.01），并减少肝脏脂质沉积，如苏木精和伊红染色所示。CHP下调HFD诱导的肥胖小鼠的PPAR γ和C/EBP α的蛋白表达，并抑制脂肪细胞分化（p < 0.01）。与HFD组相比，补充CHP具有明显的抗炎作用（降低蛋白质表达，如TNF-α、IL-6和MCP 1），降低血清和细胞中的瘦素水平和TNF-α分泌（p < 0.01）。与HFD组相比，CHP显著抑制小鼠腹膜后白色脂肪细胞中miR-27 a/B的表达（53.3%和29.9%，p < 0.01），增强靶基因Prdm 16的表达，并显著上调Sirt 1（105.5%，p < 0.01）。此外，补充CHP有效地改善了肥胖小鼠中由HFD诱导的氧化应激（ROS、T-AOC、SOD、CAT和GSH-Px）（p < 0.01）。因此，CHP减轻脂肪细胞分化、白色脂肪细胞的布朗宁、以及炎症和抗氧化活性的减少以减少肥胖。因此，这些结果为CHP在HFD诱导的肥胖中的抗肥胖作用提供了新的见解。
This study aimed to determine the anti-obesity effects and mechanisms of Cerasus humilis polyphenol (CHP) in CS7BL/6 obese mice and 3T3-L1 cells. High-performance liquid chromatography-electrospray ionization-tandem mass spectrometry was used for the qualitative and quantitative identification of CHP components. The obese mice, induced by feeding high-fat diet (HFD), were treated with CHP (250 mg/kg/day) by gavage for 12 weeks. Orlistat was gavaged at 15.6 mg/kg bw/day, as a positive control group. The analysis revealed that the main components of CHP were procyanidin B2, cyanidin-3-glucoside, and pelargonidin-3-glucoside. CHP dietary supplementation significantly reduced body weight and improved blood lipid measurements in HFD-fed mice (p < 0.01). Moreover, it inhibited mRNA expression of miR-122, Srebp-lc, and Cpt1a (p < 0.01) and reduced hepatic lipid deposition, as seen by hematoxylin and eosin staining. CHP downregulated the protein expression of PPAR gamma and C/EBP alpha in HFD-induced obese mice and inhibited adipocyte differentiation (p < 0.01). Compared with the HFD group, CHP supplementation had an obvious anti-inflammatory effect (decreased protein expression, such as TNF-alpha, IL-6, and MCP1), reducing leptin levels and TNF-alpha secretion in serum and cells (p < 0.01). CHP significantly inhibited the expression of miR-27a/b (53.3 and 29.9%, p < 0.01) in mice retroperitoneal white adipocytes, enhancing the expression of the target gene Prdm16 and significantly upregulating Sirt1 (105.5%, p < 0.01) compared with the HFD group. Moreover, CHP supplementation effectively improved oxidative stress (ROS, T-AOC, SOD, CAT, and GSH-Px) induced by HFD in obese mice (p < 0.01). Thus, CHP mitigates adipocyte differentiation, browning of white adipocytes, and reduction of inflammation and antioxidant activity to reduce obesity. Consequently, these results provide novel insights into the anti-obesity roles of CHP in HFD-induced obesity.