This study aimed to determine the anti-obesity effects and mechanisms of Cerasus humilis polyphenol (CHP) in C57BL/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-1c, and Cpt1a (p < 0.01) and reduced hepatic lipid deposition, as seen by hematoxylin and eosin staining. CHP downregulated the protein expression of PPARγ and C/EBPα 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-α, IL-6, and MCP1), reducing leptin levels and TNF-α 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.

中文翻译：

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Cerasus humilis樱桃多酚通过减轻脂肪沉积，炎症和氧化作用降低C57BL / 6小鼠的高脂饮食诱导的肥胖

这项研究的目的是为了确定Cerasus humilis多酚（CHP）在C57BL / 6肥胖小鼠和3T3-L1细胞中的抗肥胖作用及其机制。高效液相色谱-电喷雾电离串联质谱法用于CHP组分的定性和定量鉴定。通过饲喂高脂饮食（HFD）诱导的肥胖小鼠，用CHP（250 mg / kg /天）进行管饲治疗12周。将奥利司他以15.6 mg / kg体重/日灌胃，作为阳性对照组。分析显示，CHP的主要成分是原花青素B2，花青素3-葡糖苷和pelargonidin-3-葡糖苷。CHP饮食补充剂可显着降低HFD喂养小鼠的体重并改善血脂测量（p<0.01）。此外，如苏木精和曙红染色所示，它可抑制miR-122，Srebp-1c和Cpt1a的mRNA表达（p <0.01）并减少肝脂质沉积。CHP下调了HFD诱导的肥胖小鼠中PPARγ和C /EBPα的蛋白表达，并抑制了脂肪细胞的分化（p <0.01）。与HFD组相比，CHP补充剂具有明显的抗炎作用（蛋白质表达降低，例如TNF-α，IL-6和MCP1），降低了血清和细胞中的瘦素水平和TNF-α分泌（p <0.01 ）。CHP显着抑制miR-27a / b的表达（53.3和29.9％，p与HFD组相比，小鼠腹膜后白色脂肪细胞中的<0.01）增强了靶基因Prdm16的表达，并显着上调Sirt1（105.5％，p <0.01）。此外，CHP补充有效地改善了肥胖小鼠中由HFD引起的氧化应激（ROS，T-AOC，SOD，CAT和GSH-Px）（p <0.01）。因此，CHP减轻了脂肪细胞的分化，白色脂肪细胞的褐变以及减少了炎症和抗氧化活性，从而减轻了肥胖。因此，这些结果为CHP在HFD诱导的肥胖症中的抗肥胖作用提供了新颖的见解。