CAJ | 학술논문

目的：探讨微小RNA（miR）-206对apoE-／-动脉粥样硬化小鼠肝脏X受体α（LXRα）表达的影响。方法取4周龄apoE-/-小鼠30只，喂以高脂饮食，14周后随机分成对照组、miR-206 mimic组、miR-206 in-hibitor组，每组10只。尾静脉采血检测总胆固醇（TC）、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C），油红O染色观察主动脉粥样硬化程度，荧光定量聚合酶链反应（RT-PCR）测定LXRαmR-NA表达量，蛋白印迹法测定LXRα蛋白表达量。结果 miR-206 mimic组HDL-C较对照组升高；miR-206 inhi-bitor组与对照组、miR-206 mimic组相比，TC、LDL均显著升高，HDL明显下降。各组TG无明显不同。苏木精-伊红（HE）染色示对照组主动脉粥样硬化程度较轻，miR-206 inhibitor组主动脉粥样硬化程度最重，miR-206 mimic组主动脉粥样硬化病变极其微弱。miR-206 mimic组肝LXRα表达增多，而miR-206 inhibitor组表达减少。结论miR-206可能与LXRα构成反馈环，共同调节胆固醇逆转运。
목적：탐토미소RNA（miR）-206대apoE-／-동맥죽양경화소서간장X수체α（LXRα）표체적영향。방법취4주령apoE-/-소서30지，위이고지음식，14주후수궤분성대조조、miR-206 mimic조、miR-206 in-hibitor조，매조10지。미정맥채혈검측총담고순（TC）、감유삼지（TG）、고밀도지단백담고순（HDL-C）、저밀도지단백담고순（LDL-C），유홍O염색관찰주동맥죽양경화정도，형광정량취합매련반응（RT-PCR）측정LXRαmR-NA표체량，단백인적법측정LXRα단백표체량。결과 miR-206 mimic조HDL-C교대조조승고；miR-206 inhi-bitor조여대조조、miR-206 mimic조상비，TC、LDL균현저승고，HDL명현하강。각조TG무명현불동。소목정-이홍（HE）염색시대조조주동맥죽양경화정도교경，miR-206 inhibitor조주동맥죽양경화정도최중，miR-206 mimic조주동맥죽양경화병변겁기미약。miR-206 mimic조간LXRα표체증다，이miR-206 inhibitor조표체감소。결론miR-206가능여LXRα구성반궤배，공동조절담고순역전운。
Objective To investigate the effect of miR-206 on the expression of liver X receptor α (LXRα) in apoE-/-mice with atherosclerosis. Methods Thirty apoE-/-mice aged 4 weeks old were included in the study, and fed with Western diet. All mice were randomly divided into the control group, miR-206 mimic group and miR-206 in-hibitor group after 14 weeks (n=10 each). Blood samples at caudal veins were collected to measure the levels of total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C). The severity of aortic atherosclerosis was determined by red oil O staining. Levels of LXRαmRNA and pro-tein were determined by RT-PCR and Western blot, respectively. Results The HDL-C level increased in miR-206 mimic group compared with that in control group. Compared with the control group and miR-206 mimic group, signifi-cantly increased TC and LDL-C levels and decreased HDL-C level were found in miR-206 inhibitor group. There was no significant difference in TG among different groups. Red O staining showed mild aortic atherosclerosis in control group, most severe disease in the miR-206 inhibitor group, and very modest lesion of aortic atherosclerosis in the miR-206 mimic group, respectively. The LXRαexpression increased in miR-206 mimic group and decreased in miR-206 inhibitor group. Conclusion miR-206 may interact with LXRα in forming a feedback loop to regulate the reverse cholesterol transport.