Adipose tissue inflammation plays an important role in the regulation of glucose and lipids metabolism. It is unknown whether Ursolic acid (UA) could regulate adipose tissue inflammation, though it can regulate inflammation in many other tissues. In this study, 3T3-L1 adipocytes, DIO mice and lean mice were treated with UA or vehicle. Gene expression of inflammatory factors, chemokines and immune markers in adipocytes and adipose tissue, cytokines in cell culture medium and serum, and inflammation regulatory pathways in adipocytes were detected. Results showed that UA increased the expression of interleukins and chemokines, but not TNFα, in both adipocytes and adipose tissue. IL6 and MCP1 levels in the cell culture medium and mouse serum were induced by UA treatment. Cd14 expression level and number of CD14+ monocytes were higher in UA treated adipose tissue than those in the control group. Glucose tolerance test was impaired by UA treatment in DIO mice. Mechanistically, UA induced the expression of Tlr4 and the phosphorylation levels of ERK and NFκB in adipocytes. In conclusion, our study indicated that short-term UA administration could induce CD14+ monocytes infiltration by increasing the production of interleukins and chemokines in mouse adipose tissue, which might further impair glucose tolerance test.

脂肪组织炎症在糖脂代谢调节中发挥重要作用。尽管熊果酸（UA）可以调节许多其他组织的炎症，但它是否可以调节脂肪组织炎症尚不清楚。在这项研究中，3T3-L1 脂肪细胞、DIO 小鼠和瘦小鼠接受 UA 或媒介物处理。检测脂肪细胞和脂肪组织中炎症因子、趋化因子和免疫标志物的基因表达量，细胞培养基和血清中的细胞因子以及脂肪细胞中的炎症调节通路。结果表明，UA 增加了脂肪细胞和脂肪组织中白细胞介素和趋化因子的表达，但不增加 TNFα 的表达。 UA处理诱导细胞培养基和小鼠血清中IL6和MCP1水平。 UA处理的脂肪组织中Cd14表达水平和CD14+单核细胞数量高于对照组。 DIO 小鼠的葡萄糖耐量测试因 UA 治疗而受损。从机制上讲，UA 诱导脂肪细胞中 Tlr4 的表达以及 ERK 和 NFκB 的磷酸化水平。总之，我们的研究表明，短期给予UA可以通过增加小鼠脂肪组织中白细胞介素和趋化因子的产生来诱导CD14+单核细胞浸润，这可能进一步损害葡萄糖耐量测试。