Research Article

ANGPTL-3在调节HDL颗粒诱导的胆固醇外排能力中的新见解

卷 24, 期 6, 2024

发表于: 12 July, 2023

页: [771 - 779] 页: 9

弟呕挨: 10.2174/1566524023666230418104400

价格: $65

摘要

背景:血管生成素样蛋白3 (ANGPTL-3)通过抑制脂蛋白脂肪酶(LPL)调节脂质代谢和冠状动脉疾病(CAD),特别是稳定性心绞痛(SA)的风险。然而,是否有其他机制尚不清楚。本研究探讨了ANGPTL-3对高密度脂蛋白(HDL)的调节作用,从而进一步影响动脉粥样硬化的发展。 方法:共有200人参加了本研究。采用酶联免疫吸附法(ELISA)检测血清ANGPTL- 3水平。通过装载h3 -胆固醇的THP-1细胞检测HDL颗粒诱导的胆固醇外排能力。 结果:血清ANGPTL-3水平在SA组与非SA组之间无明显差异,而2型糖尿病(T2DM)组血清ANGPTL-3水平较非T2DM组显著升高[428.3 (306.2 ~ 736.8)ng/ml比298.2 (156.8 ~ 555.6)ng/ml, p <0.05]。此外,与高TG患者相比,低TG患者血清ANGPTL-3水平升高[519.9 (377.6 ~ 809.0)ng/ml vs. 438.7 (329.2 ~ 681.0) ng/ml, p <0.05]。相比之下,SA组和T2DM组均出现HDL颗粒诱导的胆固醇外排减少[SA:(12.21±2.11)% vs(15.51′}2.76)%,p <0.05;2型糖尿病:(11.24±2.13})%和(14.65±3.27})%,p < 0.05)。血清ANGPTL-3浓度与HDL颗粒胆固醇外排能力呈负相关(r=-0.184, p <0.05)。回归分析发现血清ANGPTL-3浓度是HDL颗粒胆固醇外排能力的独立调节剂(标准化β=-0.172, p <0.05)。 结论:ANGPTL-3对HDL颗粒诱导的胆固醇外排能力表现出负调节作用。

关键词: ANGPTL3,胆固醇外排能力,HDL,稳定性心绞痛,2型糖尿病,冠状动脉疾病。

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