系统性红斑狼疮患者高密度脂蛋白抗氧化能力和亚型分布及对氧磷酶1活性分析

High Density Lipoprotein Antioxidant Capacity and Subtype Distribution and Analysis of Paraoxonase-1 Activity in Patients with Systemic Lupus Erythematosus

目的探讨系统性红斑狼疮(SLE)患者高密度脂蛋白(HDL)抗氧化能力和亚型分布及对氧磷酶1(PON1)活性的相关性。方法采用常规方法检测50例SLE和50例健康对照组红细胞沉降率(ESR)、血清载脂蛋白A1(ApoA1)、高密度脂蛋白胆固醇(HDL-C)、白细胞介素(IL)-6、MCP-1、SAA等多种SLE相关标志物;采用分光光度法检测总HDL抗氧化能力;用lipoprint system分析HDL亚型;以酶水解底物对氧磷法和乙酸乙酯法检测PON1对氧磷酶活性及其芳香酯酶活性。结果与健康对照组比,SLE组HDL-C(P=0.012)和ApoA1(P=0.003)浓度显著下降;SLE组总HDL抗氧化能力(P=0.002)、HDL亚型(P<0.05)浓度、PON1芳香酯酶活性(P=0.001)显著低于对照组;SLE组hsCRP、ESR、IL-6、MCP-1、SAA显著增加(P<0.05)。SLE组HDL-C和总HDL抗氧化能力与PON1芳香酯酶活性及PON1对氧磷酶活性成正相关(P<0.05),与ESR、hsCRP、IL-6、MCP-1、SAA呈负相关(P<0.05),其中PON1芳香酯酶活性和ESR与总HDL抗氧化能力最具相关性。结论 HDL抗氧化能力及PON1活性降低、HDL亚型改变、系统性炎症增加等多因素可能导致SLE患者动脉粥样硬化风险的增加。

Objective In order to investigate the relationship between systemic lupus erythematosus （SLE） and high-density lipoprotein （HDL） antioxidant capacity, HDL subfractions, paraoxonase-1 （PON1） activity. Methods Several factors, including ESR, ApoA1, HDL-C, IL-6, MCP-1 and SAA were determined by normal methods in 50 SLE patients and 50 healthy controls. HDL antioxidant capacity was determined spectrophotometrical method. Lipoprint system was used for HDL subfraction analysis. PON1 paraoxonase activity and arylesterase activity analyzed using paraoxon and phenylacetate as the substrate. Results Compared with healthy controls, HDL-C （P=0.012） and ApoA1 （P=0.003） concentrations decreased significantly in SLE subjects. Total HDL antioxidant capacity （P=0.002）, HDL subfractions （P〈O.05） and PON1 arylesterase activity （P--0.001） were significantly reduced in SLE patients. The levels of hsCRP, ESR, IL-6, MCP-1 and SAA were significantly elevated in SLE patients （P〈0.05）. HDL-C and total HDL antioxidant capacity correlated positively with PON 1 paraoxonase activity and arylesterase activity, and negatively with hsCRP, ESR, IL-6, MCP-1 and SAA, respectively. PON1 aryl esterase activity and ESR were independent predictors of total HDL antioxidant capacity. Conclusion Reduction of HDL antioxidant and PON1 activity, alteration of subfractions distribution and inflammation may contribute to the increased atherosclerosis risk of SLE patients.