Department of Marine Life Sciences, Jeju National University, Jeju 63243, Korea.
Korea Food Research Institute, 245 Nongsaengmyeong-Ro Iseo-Myeon, Wanju-Gun, Jeollabuk-Do 55365, Korea.
Mar Drugs. 2019 Jan 10;17(1):44. doi: 10.3390/md17010044.
The purpose of this study was to investigate the antiobesity effect and the mechanism of action of diphlorethohydroxycarmalol (DPHC) isolated from in 3T3-L1 cells. The antiobesity effects were examined by evaluating intracellular fat accumulation in Oil Red O-stained adipocytes. Based on the results, DPHC dose-dependently inhibited the lipid accumulation in 3T3-L1 adipocytes. DPHC significantly inhibited adipocyte-specific proteins such as SREBP-1c, PPARγ, C/EBP α, and adiponectin, as well as adipogenic enzymes, including perilipin, FAS, FABP4, and leptin in adipocytes. These results indicated that DPHC primarily acts by regulating adipogenic-specific proteins through inhibiting fat accumulation and fatty acid synthesis in adipocytes. DPHC treatment significantly increased both AMPK and ACC phosphorylation in adipocytes. These results indicate that DPHC inhibits the fat accumulation by activating AMPK and ACC in 3T3-L1 cells. Taken together, these results suggest that DPHC can be used as a potential therapeutic agent against obesity.
本研究旨在探讨从 中分离得到的二氢二羟基卡瓦醇（DPHC）在 3T3-L1 细胞中的抗肥胖作用及其作用机制。通过评估油红 O 染色脂肪细胞中的细胞内脂肪积累来检测抗肥胖作用。结果表明，DPHC 剂量依赖性地抑制了 3T3-L1 脂肪细胞中的脂质积累。DPHC 还显著抑制了脂肪细胞特异性蛋白，如 SREBP-1c、PPARγ、C/EBPα和脂联素，以及脂肪生成酶，包括脂滴包被蛋白、脂肪酸合成酶、脂肪细胞型脂肪酸结合蛋白 4 和瘦素。这些结果表明，DPHC 主要通过调节脂肪生成特异性蛋白来抑制脂肪细胞中的脂肪积累和脂肪酸合成。DPHC 处理显著增加了脂肪细胞中 AMPK 和 ACC 的磷酸化。这些结果表明，DPHC 通过激活 3T3-L1 细胞中的 AMPK 和 ACC 来抑制脂肪积累。综上所述，这些结果表明 DPHC 可作为一种治疗肥胖的潜在药物。
