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

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。

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.