Liu G X, Ou D M, Liu J H, Huang H L, Liao D F
Department of Pharmacology, Hengyang Medical College, Hengyang 421001, China.
Acta Pharmacol Sin. 2000 Jul;21(7):637-40.
To investigate the mechanisms of anti-atherogenic actions of probucol.
Human peripheral blood monocytes were cultured, and treated by copper ion (10 mumol/L) and/or probucol (PBC). Lipid peroxidation was measured by assaying malondialdehyde (MDA). The cytokine interleukin-1 beta (IL-1 beta) and apolipoprotein E (apo E) secreted by monocyte were assayed by enzyme linked immunoassay (ELISA).
PBC 10-80 mumol/L inhibited copper ion-induced cellular lipid peroxidation from 15.30 to 7.74 mumol MDA/g cell protein. PBC 40 mumol/L inhibited oxidized macrophage-mediated oxidation of LDL from 5.18 to 1.65 mumol MDA/g cell protein, and attenuated secretory properties of monocytes induced by copper ion. The release of apo E, which is involved in reverse cholesterol transport, increased by 65%. And the release of IL-1 beta, which was shown to enhance vascular smooth muscle cell proliferation, decreased by 45%.
Probucol inhibits lipid peroxidation of macrophages and affects their secretory properties.
研究普罗布考的抗动脉粥样硬化作用机制。
培养人外周血单核细胞，并用铜离子（10 μmol/L）和/或普罗布考（PBC）进行处理。通过测定丙二醛（MDA）来检测脂质过氧化。采用酶联免疫吸附测定法（ELISA）检测单核细胞分泌的细胞因子白细胞介素-1β（IL-1β）和载脂蛋白E（apo E）。
10 - 80 μmol/L的PBC可将铜离子诱导的细胞脂质过氧化从15.30 μmol MDA/g细胞蛋白抑制至7.74 μmol MDA/g细胞蛋白。40 μmol/L的PBC可将氧化型巨噬细胞介导的低密度脂蛋白（LDL）氧化从5.18 μmol MDA/g细胞蛋白抑制至1.65 μmol MDA/g细胞蛋白，并减弱铜离子诱导的单核细胞分泌特性。参与逆向胆固醇转运的apo E释放增加了65%。而可增强血管平滑肌细胞增殖的IL-1β释放减少了45%。
普罗布考可抑制巨噬细胞的脂质过氧化并影响其分泌特性。
