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目的:研究丙丁酚(probucol,PBC)的抗动脉粥样硬化机理。方法:采用Cu~(2+)(10μmol/L)处理巨噬细胞,并观察了丙丁酚对巨噬细胞脂质过氧化及其介导的低密度脂蛋白氧化的抑制作用和对巨噬细胞分泌功能的影响。结果:10-80μmol/L PBC能抑制Cu~(2+)诱导的巨噬细胞脂质过氧化(MDA从15.30抑制到7.74μmol/g cell protein,P<0.01),且PBC处理的巨噬细胞介导的低密度脂蛋白氧化较对照组低(MDA从5.18到1.65μmol/g cell protein,P<0.05)。PBC对Cu~(2+)诱导的巨噬细胞分泌IL-1β抑制45％,apo E分泌增加65％。结论:丙丁酚在体外能抑制巨噬细胞脂质过氧化及其介导的低密度脂蛋白氧化,并调节巨噬细胞的分泌功能。
Objective: To study the anti-atherosclerotic mechanism of probucol (PBC). Methods: Macrophages were treated with Cu (2 +) (10μmol / L), and the inhibitory effect of probucol on lipid peroxidation and LDL-induced oxidative inhibition of macrophages and the effect on macrophage The effect of secretion. Results: 10-80μmol / L PBC could inhibit the Cu 2+ -induced macrophage lipid peroxidation (MDA inhibited from 15.30 to 7.74μmol / g cell protein, P <0.01), and PBC-treated macrophages LDL oxidation was lower than that of the control group (MDA ranged from 5.18 to 1.65 μmol / g cell protein, P <0.05). PBC inhibited 45% secretion of IL-1β and increased apo E secretion by Cu 2+ -mediated macrophages by 65%. CONCLUSION: Probucol can inhibit macrophage lipid peroxidation and its mediated LDL oxidation and regulate macrophage secretion in vitro.