肥胖症被認為與代謝症候群有密切關係，肥胖者容易誘發糖尿病與心血管相關疾病。另外，肥胖也被視為一種慢性發炎反應，所以減少脂肪細胞發炎反應，將有助於減少肥胖所衍生的疾病。前人研究發現蜂膠具有抑制脂多醣(LPS) 誘導發炎的巨噬細胞分泌IL-6，本實驗目標在探討蜂膠對於脂肪細胞分泌發炎相關趨化激素的調控作用，並討論相關的分子機制。分化後的小鼠脂肪細胞株(3T3-L1)，經由不同劑量的蜂膠處理後給予脂多醣刺激，分析趨化激素(CCL5 及MCP-1) 之釋放量及COX-2、磷酸化IκB-α、NF-κB 蛋白質之表現及MAPK 訊息路徑的變化。結果發現，蜂膠具有顯著抑制CCL5 及MCP-1 趨化激素的分泌效力，並且會減弱COX-2 的表現。觀察NF-κB 路徑發現，經蜂膠處理的發炎3T3-L1 脂肪細胞，藉著抑制IκB-α 的磷酸化，導致NF-κB 的次單位p65 無法移動入細胞核，進而調控發炎基因之轉錄作用。另外，MAPK 路徑中，磷酸化的ERK、p38 及JNK 的表現也顯著的減少。由上述結果發現，蜂膠之抗發炎效應，可能透過抑制3T3-L1 脂肪細胞趨化激素(CCL5 及MCP-1) 之分泌，同時會降低COX-2 的表現。b

Obesity is an important indicator of the metabolic syndrome. Obesity may induce diabetes and cardiovascular disease. In addition, obesity is a chronic inflammatory response, and reducing the inflammation of adipocytes will decrease the probability of diseases derived from obesity. The previous study found that propolis could inhibit the IL-6 level in LPS-induced macrophages. This study aims to and MCP-1), COX-2, phosphorylation of IB-α, and NF-B proteins and the MAPK signaling pathway in 3T3-L1 adipocytes. Pretreatment with propolis significantly inhibited the expression of chemokines (CCL5 and MCP-1) and COX-2 protein. In addition, we found that propolis suppressed the nuclear translocation of NF-B and decreased the phosphorylation of ERK, p38 and JNK. These results suggest that propolis exerts anti-inflammatory effects through the inhibition of chemokines and COX-2 expression in 3T3-L1 adipocytes.