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作 者:黎雪芳 李志军[1] 叶健 叶武 Li Xuefang
机构地区:[1]浙江医院,310013
出 处:《浙江临床医学》2025年第1期8-10,共3页Zhejiang Clinical Medical Journal
基 金:浙江省医药卫生科技计划项目(2022KY012)。
摘 要:目的 探讨荜茇酰胺对肺动脉内皮细胞内皮间质转化的影响。方法 根据不同干预方式将肺动脉内皮细胞和Wistar大鼠分为常氧组、低氧组和荜茇酰胺组,采用CCK-8法检测细胞存活率,蛋白质印迹法检测间质标志物α-SMA和内皮标志蛋白E-Cadherin的表达水平,比较各组大鼠右心室收缩压和右心室肥厚指数。结果 荜茇酰胺抑制肺动脉内皮细胞增殖(P<0.05)。低氧组和荜茇酰胺组肺动脉内皮细胞和大鼠肺组织α-SMA和E-Cadherin蛋白表达水平比较,差异有统计学意义(P<0.05)。低氧组和荜茇酰胺组大鼠右心室收缩压和右心室肥厚指数比较,差异有统计学意义(P<0.05)。结论 荜茇酰胺可抑制肺动脉内皮细胞内皮间质转化。Objective To investigate the effect of piperlongamide on endothelial-mesenchymal transition(EMT)in pulmonary artery endothelial cells(PAecs).Methods Pulmonary artery endothelial cells and Wistar rats were divided into the normoxia group,hypoxia the group and the piperlongumine group according to different intervention methods.CCK-8 method was used to detect cell viability.The right ventricular systolic pressure and right ventricular hypertrophy index were compared among the groups.Results Piperlongamide inhibited the proliferation of pulmonary artery endothelial cells(P<0.05).The protein expression levels of α-SMA and E-Cadherin in pulmonary artery endothelial cells and lung tissue of rats in the hypoxia group and the piperlongamide group were significantly different(P<0.05).There were significant differences in right ventricular systolic pressure and right ventricular hypertrophy index between the hypoxia group and the piperlongamide group(P<0.05).Conclusion Piperlongamide can inhibit the endothelialmesenchymal transition of pulmonary artery endothelial cells.
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