CAJ | 학술논문

目的：建立金黄地鼠高脂血症模型，并对胆固醇代谢紊乱的分子机制进行探讨。方法金黄地鼠随机分为正常和模型组，正常组饲常规饲料，模型组饲高脂饲料，连续诱导4周。酶法检测血脂水平和 CYP7A1活性，荧光实时定量PCR技术探讨金黄地鼠高脂血症模型胆固醇代谢紊乱的分子机制。结果金黄地鼠经高脂饲料诱导后与对照组比较，血清TC、LDL-C和TG明显升高，肝脏TC、TG明显增加。机制研究表明，模型组 CYP7A1活性明显降低，肝脏 LDL-R、SREBP-2、CYP7A1和LXRα表达下调，肝脏FXR表达上调。结论金黄地鼠经高脂饲料诱导后可形成以TC、LDL-C、TG升高为特征的高脂血症模型， LDL-R、SREBP-2、CYP7A1、FXR和LXRα既是金黄地鼠高脂血症模型胆固醇代谢紊乱的生物标志物，也是抗高胆固醇血症药物的作用靶标。
목적：건립금황지서고지혈증모형，병대담고순대사문란적분자궤제진행탐토。방법금황지서수궤분위정상화모형조，정상조사상규사료，모형조사고지사료，련속유도4주。매법검측혈지수평화 CYP7A1활성，형광실시정량PCR기술탐토금황지서고지혈증모형담고순대사문란적분자궤제。결과금황지서경고지사료유도후여대조조비교，혈청TC、LDL-C화TG명현승고，간장TC、TG명현증가。궤제연구표명，모형조 CYP7A1활성명현강저，간장 LDL-R、SREBP-2、CYP7A1화LXRα표체하조，간장FXR표체상조。결론금황지서경고지사료유도후가형성이TC、LDL-C、TG승고위특정적고지혈증모형， LDL-R、SREBP-2、CYP7A1、FXR화LXRα기시금황지서고지혈증모형담고순대사문란적생물표지물，야시항고담고순혈증약물적작용파표。
Aim To establish the hyperlipidemic model and ex-plore the mechanism of hypercholesterolemia in hamster. Meth-ods Hamsters were randomly divided into the control and model groups. The hamsters in the control group were fed with the standard chow and the model group were fed with the high fat di-et. Serum lipids and CYP7A1 activity were detected by enzymat-ic method. The molecular mechanism of cholesterol metabolism was investigated by real-time PCR. Results In comparison with the control group, the concentrations of serum TC, LDL-C, TG and hepatic TC, TG were significantly increased in the model <br> group. The mechanism research showed that in hamsters fed with the high fat diet, the CYP7A1 activity and the mRNA expres-sions of hepatic LDL-R, SREBP-2, CYP7A1, LXRαwere down-regulated, the expression of hepatic FXR was up-regulated. Conclusion The hyperlipidemic model could be developed in hamsters fed with the high fat diet for 4 weeks. LDL-R, SREBP-2, CYP7A1, FXR and LXRαare the biomarkers of hypercholes-terolemia, and also the targets of hypolipidemic drugs.