Division of Cardiovascular Research, University of Manchester, Oxford Road, Manchester M13 9WL, UK.
IUBMB Life. 2012 Feb;64(2):157-61. doi: 10.1002/iub.588. Epub 2011 Dec 20.
The inhibition of low-density lipoprotein (LDL) oxidation by high-density lipoprotein (HDL) is a major antiatherogenic property of this lipoprotein. This activity is due, in part, to HDL associated proteins. However, whether these proteins interact in the antioxidant activity of HDL is unknown. LDL was incubated with apolipoprotein A1 (apo A1), lecithin:cholesterol acyltransferase (LCAT), and paraoxonase-1 (PON1) alone or in combination, in the presence or absence of HDL under oxidizing conditions. LDL lipid peroxide concentrations were determined. Apo A1, LCAT, and PON1 all inhibit LDL oxidation in the absence of HDL and enhance the ability of HDL to inhibit LDL oxidation. Their effect was additive rather than synergistic; the combination of these proteins significantly enhanced the length of time LDL was protected from oxidation. This seemed to be due to the ability of PON1 to prevent the oxidative inactivation of LCAT. Apo A1, LCAT, and PON1 can all contribute to the antioxidant activity of HDL in vitro. The combination of apo A1, LCAT, and PON1 prolongs the time that HDL can prevent LDL oxidation, due, at least in part, to the prevention LCAT inactivation.
高密度脂蛋白 (HDL) 抑制低密度脂蛋白 (LDL) 氧化是该脂蛋白主要的抗动脉粥样硬化特性。这种活性部分归因于与 HDL 相关的蛋白质。然而，这些蛋白质是否在 HDL 的抗氧化活性中相互作用尚不清楚。在氧化条件下，将 LDL 与载脂蛋白 A1 (apo A1)、卵磷脂：胆固醇酰基转移酶 (LCAT) 和对氧磷酶-1 (PON1) 单独或组合孵育，存在或不存在 HDL。测定 LDL 脂质过氧化物浓度。apo A1、LCAT 和 PON1 在没有 HDL 的情况下均可抑制 LDL 氧化，并增强 HDL 抑制 LDL 氧化的能力。它们的作用是相加的，而不是协同的；这些蛋白质的组合显著延长了 LDL 免受氧化的时间。这似乎是由于 PON1 能够防止 LCAT 的氧化失活。apo A1、LCAT 和 PON1 均可在体外促进 HDL 的抗氧化活性。apo A1、LCAT 和 PON1 的组合延长了 HDL 可以防止 LDL 氧化的时间，至少部分原因是防止了 LCAT 的失活。
