中文摘要：

目的探讨氧化低密度脂蛋白（ox LDL）促进血管平滑肌细胞（vascular smooth muscle cells,VSMCs）泡沫化是否与过氧化物酶体增殖物激活受体γ（peroxisome proliferator-activated receptorγ,PPARγ）-三磷酸腺苷结合盒转运子G1（ATP-binding cassette transporter G1,ABCG1）通路调节相关。方法组织贴块法培养原代VSMCs;细胞免疫荧光染色鉴定原代VSMCs;BODIPY染色定性检测细胞内脂质沉积,酶促比色法定量检测细胞内总胆固醇沉积的量;Western blot检测VSMCs中PPARγ、ABCG1蛋白表达情况。结果 1Ox LDL作用VSMCs 48 h后脂质沉积增加;2Ox LDL作用VSMCs PPARγ蛋白表达量下降约53%（P〈0.01）,ABCG1蛋白表达量下降约48%（P〈0.05）;3罗格列酮激动PPARγ后,ABCG1蛋白表达量较单独的ox LDL组增加约147%（P〈0.05）,VSMCs中脂质沉积明显减少。结论ox LDL通过PPARγ-ABCG1通路促进血管平滑肌细胞泡沫化。

英文摘要：

Objective To investigate whether oxidized low-density lipoprotein（ ox LDL） promoting vascular smooth muscle cells（ VSMCs） to form foam cells is regulated by peroxisome proliferator receptor γ（ PPARγ）-ATP-binding cassette transporter G1（ ABCG1） pathway. Methods Primary VSMCs were isolated from male C57 BL /6J mice,cultured with tissue explant technique,and identified by immunofluorescence staining. BODIPY staining was used to analyze the intracellular lipid deposition,and the total cholesterol deposition in the VSMCs was quantitatively detected by enzymatic colorimetric assay. the protein expression of PPARγ and ABCG1 in the VSMCs was analyzed by Western blotting. Results After ox LDL intervention in the VSMCs for 48 h,the lipid deposition was increased. PPARγ protein expression was decreased by about53%（ P〈 0. 01）,while ABCG1 protein expression was decreased by about 48%（ P〈 0. 05）. After rosiglitazone activated PPARγ,ABCG1 protein expression was increased by about 147%（ P〈 0. 05）,and the lipid deposition was reduced in the VSMCs. Conclusion Ox LDL promotes the formation of smooth musclederived foam cells through PPARγ-ABCG1 signal pathway.