Ethyl gallate (EG) is a well-known constituent of medicinal plants, but its effects on atherosclerosis development are not clear. In the present study, the anti-atherosclerosis effects of EG and the underlying mechanisms were explored using macrophage cultures, zebrafish and apolipoprotein (apo) E deficient mice. Treatment of macrophages with EG (20 μM) enhanced cellular cholesterol efflux to HDL, and reduced net lipid accumulation in response to oxidized LDL. Secretion of monocyte chemotactic protein-1 (MCP-1) and interleukin-6 (IL-6) from activated macrophages was also blunted by EG. Fluorescence imaging techniques revealed EG feeding of zebrafish reduced vascular lipid accumulation and inflammatory responses in vivo. Similar results were obtained in apoE^-/- mice 6.5 months of age, where plaque lesions and monocyte infiltration into the artery wall were reduced by 70% and 42%, respectively, after just 6 weeks of injections with EG (20 mg/kg). HDL-cholesterol increased 2-fold, serum cholesterol efflux capacity increased by ∼30%, and the levels of MCP-1 and IL-6 were reduced with EG treatment of mice. These results suggest EG impedes early atherosclerosis development by reducing the lipid and macrophage-content of plaque. Underlying mechanisms appeared to involve HDL cholesterol efflux mechanisms and suppression of pro-inflammatory cytokine secretion.

没食子酸乙酯（EG）是药用植物的众所周知的成分，但其​​对动脉粥样硬化发展的影响尚不清楚。在本研究中，使用巨噬细胞培养物，斑马鱼和载脂蛋白（apo）E缺陷型小鼠探索了EG的抗动脉粥样硬化作用及其潜在机制。用EG（20μM）处理巨噬细胞可增强细胞对HDL的胆固醇外流作用，并减少对氧化LDL的净脂质蓄积。EG也抑制了活化巨噬细胞分泌单核细胞趋化蛋白1（MCP-1）和白介素6（IL-6）。荧光成像技术显示斑马鱼的EG喂养减少了体内血管脂质的积累和炎症反应。在apoE中获得了类似的结果^{- /-}在6.5个月大的小鼠中，仅用EG（20 mg / kg）注射6周后，斑块损伤和单核细胞向动脉壁的浸润分别减少了70％和42％。HDL-胆固醇增加了2倍，血清胆固醇外排能力增加了约30％，而EG处理小鼠降低了MCP-1和IL-6的水平。这些结果表明，EG通过减少斑块的脂质和巨噬细胞含量而阻碍了早期的动脉粥样硬化的发展。潜在的机制似乎涉及HDL胆固醇外排机制和促炎性细胞因子分泌的抑制。