长链非编码RNA-p21诱导细胞凋亡在动脉粥样硬化中的作用  

The effect of long non-codingRNA-p21-induced apoptosis in atherosclerosis

作　　者：尹来波[1] 刘瑞英 侯量[1] 胡思远[1] 朱志军[1] 朱佳龙[1] 

机构地区：[1]石河子大学医学院第一附属医院心胸外一科,新疆石河子832008 [2]山东省潍坊市市直机关医院超声科,山东潍坊261061

出　　处：《东南大学学报（医学版）》2017年第5期816-821,共6页Journal of Southeast University(Medical Science Edition)

摘　　要：目的:探讨lincRNA-p21通过调控细胞凋亡参与冠心病的发生发展过程,及其对动脉粥样硬化的影响。方法:选取我院50例冠心病患者,用El ISA方法检测患者血清中lincRNA-p21含量和凋亡蛋白Bcl-2含量。提取大鼠心肌内皮细胞制备大鼠动脉硬化模型,过表达或抑制lincRNA-p21后,CCK-8法检测细胞存活率;构建lincRNA-p21质粒注射进入小鼠颈动脉损伤模型,HE染色观察小鼠颈动脉内膜新生。Caspase-3活性检测试剂盒检测内皮细胞凋亡蛋白Caspase-3活性;Western blot法检测凋亡蛋白Bcl-2和BAX蛋白表达水平。结果:冠心病患者血清内lincRNA-p21表达显著下降,差异有统计学意义(P<0.05)。大鼠原代内皮细胞中过表达lincRNA-p21显著降低细胞存活率,显著上升Caspase-3活性,显著增加BAX表达,显著下降BCL-2表达;lincRNA-p21抑制组细胞存活率明显增高,Caspase 3活性显著下降,促凋亡蛋白BAX水平显著降低,抗凋亡蛋白BCL-2水平显著增加,差异有统计学意义(P<0.05)。小鼠体内局部沉默lincRNA-p21后,血管内/中膜厚度比明显增加,Caspase-3活性明显降低,Bcl-2蛋白表达增加且BAX蛋白表达降低,差异有统计学意义(P<0.05)。结论:lincRNA-p21可通过调控细胞凋亡参与冠心病的发生发展过程。Objective： To investigate the effect of lincRNA-p21 on the development of coronary heart disease（CHD） via regulating apoptosis.Methods： Fifty patients with coronary heart disease were randomly divided into two groups.The content of lincRNA-p21 and the content of apoptotic protein BCL-2 were detected through ELISA method.Rat cardiac endothelial cells were extracted to prepare for rat arteriosclerosis model with overexpression or inhibition of lincRNA-p21,followed by the detection of cell viability using CCK-8 method.LincRNA-p21 plasmid was constructed and implanted into the mice carotid artery injury model,Carotid artery neointima in mice was detected by HE staining.Caspase 3 activity assay kit was used to detect the expression of Caspase 3 in endothelial cells.The expression of BCL-2 and BAX protein was detected by Westernblot.Result： The expression of lincRNA-p21 in serum of patients with coronary heart disease was significantly decreased（P〈0.05）.The cell viability of lincRNAp21 overexpression in rat primary endothelial cells was significantly reduced,Caspase 3 activity was significantly increased,BAX protein expression was significantly increased,and BCL-2 protein expression was significantly decreased.LincRNA-p21 inhibation was significantly increased the cell survival,Caspase 3 activity was significantly decreased,the level of pro-apoptotic protein BAX was significantly decreased,anti-apoptotic protein BCL-2 levels increased significantly,the difference was statistically significant（P〈0.05）.Intravascular/medial thickness ratio was increased significantly after mice localized with lincRNA-p21 inhibition,Caspase 3 activity was significantly decreased,Bcl-2 protein expression was increased and BAX protein expression was decreased,the difference was statistically significant（P〈0.05）.Conclusion： lincRNA-p21 could be involved in the development of coronary heart disease by regulating apoptosis.

关 键 词：lincRNA-p21 冠心病 细胞凋亡 BCL-2 

分 类 号：R541.4[医药卫生—心血管疾病]