Department of Emergency Medicine, Tri-Service General Hospital, National Defense Medical Center , Taipei, Taiwan, R.O.C.
Graduate Institute of Injury Prevention and Control, College of Public Health and Nutrition, Taipei Medical University , Taipei, Taiwan, R.O.C.
J Agric Food Chem. 2017 Apr 19;65(15):3141-3150. doi: 10.1021/acs.jafc.6b05832. Epub 2017 Apr 10.
Foam cells are formed when macrophages imbibe low-density lipoprotein (LDL) through scavenger receptors. Here we examined how epigallocatechin-3-gallate (EGCG) influences foam cell formation. We found that EGCG dose-dependently reduced oxidized LDL (oxLDL) uptake in THP-1 (10 μM, 20.0 ± 0.50, p < 0.05) and primary macrophages (134.6 ± 15.6, p < 0.05) and reduced intracellular cholesterol content in these cells, respectively (10 μM, 32.6 ± 0.14, p < 0.05; 31.7 ± 1.26, p < 0.05). EGCG treatment decreased scavenger receptor A expression, but not the expression of CD36 or of reverse cholesterol transporters. Moreover, EGCG stimulated translocation of the p50 and p65 subunits of NF-κB and enhanced NF-κB DNA-binding activity, thus suppressing SR-A promoter activity. EGCG's suppression of SR-A expression was blocked by the NF-κB inhibitor Bay. The present findings suggest that EGCG regulates NF-κB activity and thus suppresses SR-A expression, oxLDL uptake, and foam cell formation.
泡沫细胞是巨噬细胞通过清道夫受体吞噬低密度脂蛋白（LDL）形成的。在这里，我们研究了表没食子儿茶素没食子酸酯（EGCG）如何影响泡沫细胞的形成。我们发现 EGCG 剂量依赖性地降低了 THP-1（10 μM，20.0 ± 0.50，p < 0.05）和原代巨噬细胞（134.6 ± 15.6，p < 0.05）摄取氧化型 LDL（oxLDL）的能力，并分别降低了这些细胞内的胆固醇含量（10 μM，32.6 ± 0.14，p < 0.05；31.7 ± 1.26，p < 0.05）。EGCG 处理降低了清道夫受体 A 的表达，但不影响 CD36 或胆固醇逆转运蛋白的表达。此外，EGCG 刺激了 NF-κB 的 p50 和 p65 亚基的易位，并增强了 NF-κB 的 DNA 结合活性，从而抑制了 SR-A 启动子活性。NF-κB 抑制剂 Bay 阻断了 EGCG 对 SR-A 表达的抑制作用。这些发现表明，EGCG 调节 NF-κB 活性，从而抑制 SR-A 表达、oxLDL 摄取和泡沫细胞形成。
