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目的探讨小鼠血管平滑肌细胞(vascular smooth muscle cells,VSMCs)在机械牵张力(stretch stress,SS)和氧化低密度脂蛋白(oxidized low-density lipoprotein,ox LDL)作用下全基因组甲基化水平的变化,并进一步考察辛伐他汀(simvastatin,SIM)对此变化的影响。方法血浆制备氧化型低密度脂蛋白,体外常规培养VSMCs,施加机械牵张力和/或氧化型低密度脂蛋白,或用辛伐他汀预处理1h后再施加刺激,用荧光探针5-甲基胞嘧啶检测VSMCs全基因组甲基化水平。以细胞免疫荧光定量阳性率和SPSS统计软件对甲基化水平进行分析。结果机械牵张力和氧化型低密度脂蛋白均可降低VSMCs的全基因组甲基化水平,且两者联合作用大于单一因素,辛伐他汀预处理VSMCs可部分抑制机械牵张力和/或氧化低密度脂蛋白诱导的全基因组甲基化水平降低。结论机械牵张力和氧化低密度脂蛋白可分别促进VSMCs全基因组甲基化水平降低,当两者共处理时呈相加作用,辛伐他汀可部分抑制上述效应。
Objective To investigate the methylation level of whole genome of mouse vascular smooth muscle cells (VSMCs) under the influence of stretch stress (SS) and oxidized low-density lipoprotein (ox LDL) Changes, and further investigate the impact of simvastatin (SIM) on this change. Methods Oxidized low density lipoprotein (LDL) was prepared in plasma. VSMCs were cultured in vitro. Mechanical stretch and / or oxidized low density lipoprotein (LDL) was stimulated with simvastatin for 1 h. Cytosine detection of whole genome methylation of VSMCs. The level of methylation was analyzed by quantitative immunofluorescence and SPSS statistical software. Results Both mechanical stretch and oxidized low density lipoprotein (LDL) decreased the whole genome methylation level of VSMCs, and the combination of them was more than a single factor. Simvastatin pretreated VSMCs could partially inhibit mechanical stretch and / or oxidative low density Lipoprotein-induced genome-wide methylation levels are reduced. Conclusion Mechanical stretch and oxidized low density lipoprotein (LDL) can promote the reduction of whole genome methylation of VSMCs respectively. When both of them are co-treated, simvastatin can partially inhibit the above effects.