lnc-MRGPRF-6:1对动脉粥样硬化中巨噬细胞脂质代谢的影响

尤志欢; 梁小洁; 王文平; 梁彩虹

doi:10.12125/j.chj.202207104

lnc-MRGPRF-6:1对动脉粥样硬化中巨噬细胞脂质代谢的影响

Role of lnc-MRGPRF-6:1 in macrophages lipid metabolism in atherosclerosis

摘要

摘要:
目的研究长链非编码RNA MRGPRF-6:1（lnc-MRGPRF-6:1）对动脉粥样硬化中脂质代谢影响。
方法收集临床资料，通过逆转录-聚合酶链式反应(qRT-PCR) 测定对照组（n=20）和冠状动脉粥样硬化性心脏病（coronary artery disease，CAD ）组（n=20）血浆中lnc-MRGPRF-6:1的表达，通过试剂盒检测对照组和CAD组的总胆固醇（total cholesterol, TC）、甘油三酯（triglyceride, TG）含量，分析lnc-MRGPRF-6:1与TC、TG的相关性。构建lnc-MRGPRF-6:1敲减的THP-1源性的巨噬细胞模型，以阴性对照慢病毒感染细胞作为对照，进行油红染色，检测TC、TG、丙二醛（malondialdehyde , MDA）、活性氧（reactive oxygen species , ROS）含量、超氧化物歧化酶（superoxide dismutase, SOD）活性，CCK-8检测细胞活性，流式细胞术分析细胞凋亡。
结果 CAD患者血浆中lnc-MRGPRF-6:1、TC、TG的表达量显著高于对照组（P<0.05），且lnc-MRGPRF-6:1的表达与TC、TG表达呈正相关。lnc-MRGPRF-6:1敲减细胞中脂质积聚减少，TC、TG、MDA、ROS含量显著下降（P<0.05），SOD的活性明显改善（P<0.05），细胞活性明显提高（P<0.05）且凋亡减少。
结论 lnc-MRGPRF-6:1可促进巨噬细胞中脂质积聚、脂质过氧化。

Abstract:
AIM To investigate the role of long non-coding RNA MRGPRF-6:1 (lnc-MRGPRF-6:1) in macrophages lipid metabolism in atherosclerosis.
METHODS The expression of lnc-MRGPRF-6:1 in plasma of control group (n=20) and coronary artery disease (CAD) patients (n=20) was measured by reverse transcription polymerase chain reaction (qRT-PCR). Commercial kits were used to detect The content of total cholesterol (TC) and triglyceride (TG) were detected in all patients and control group and the correlation between lnc-MRGPRF-6:1 and TC and TG was analyzed. Subsequently, we constructed lnc-MRGPRF-6:1 knockdown macrophages and control group macrophages respectively. The content of TC, TG, malondialdehyde (MDA) and reactive oxygen species (ROS) and the activity of superoxide dismutase (SOD) in macrophages were measured by commercial kits. Cell viability was detected by CCK-8 and cell apoptosis was analyzed by flow cytometry.
RESULTS The expression of lnc-MRGPRF-6:1 and the content of TC and TG in the plasma of CAD patients were significantly increased (P<0.05) and the expression of lnc-MRGPRF-6:1 was positively correlated with the content of TC and TG. After the knockdown of lnc-MRGPRF-6:1, the lipid accumulation of macrophages decreased significantly. Meanwhile, the content of TC, TG, MDA and ROS was significantly decreased (P<0.05), the activity of SOD increased remarkably (P<0.05), the cell viability was improved extremely (P<0.05) and cell apoptosis was decreased in the lnc-MRGPRF-6:1 knockdown macrophages.
CONCLUSION lnc-MRGPRF-6:1 accelerates lipid accumulation and lipid peroxidation in macrophages of atherosclerosis.

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