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姜黄素下调miR-21表达缓解ox-LDL诱导的血管内皮细胞损伤

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摘要:

目的 探究姜黄素调控微小RNA-21(miR-21)表达,减轻氧化低密度脂蛋白(ox-LDL)
诱导血管内皮(VE)细胞损伤的生物学机制。方法 将VE细胞分为空白组、模型组(100 μg/ml ox-
LDL)和姜黄素组(100 μg/ml ox-LDL+50 μg/ml姜黄素)。采用CCK-8法检测VE细胞增殖能力,伤口
愈合实验和Transwell实验分别检测各组细胞增殖、迁移和侵袭能力。实时荧光定量PCR(RT-qPCR)或
Western blot评估各组细胞中增殖细胞核抗原(PCNA)和基质金属蛋白酶9(MMP-9)的mRNA和蛋白表
达水平,以及miR-21的表达水平。结果 采用不同浓度ox-LDL处理组细胞存活率均明显下降,其中使用
100 μg/mL ox-LDL处理VE细胞的存活率为(58.916±3.138)%,该浓度用于构建血管内皮细胞损伤模
型。模型组VE细胞增殖活力(P<0.01),迁移能力[(33.063±3.532)vs.(64.397±4.648),P<0.01]
和侵袭能力[(256.667±11.865)vs.(404.333±10.105),P<0.01]均低于空白组;姜黄素组VE细胞增殖
活力(P<0.01)、迁移能力(61.773±2.451,P<0.01)和侵袭能力[(393.000±11.547),P<0.01]均
高于模型组。模型组PCNA(P<0.01)和MMP-9(P<0.01)的mRNA及蛋白表达水平均低于空白组;姜
黄素组PCNA(P<0.01)和MMP-9(P<0.01)的mRNA及蛋白表达水平均高于模型组。另外,miR-21在
模型组中的相对表达量为(8.020±0.483),高于空白组(P<0.01);miR-21在姜黄素组中的相对表达
量为(2.241±0.205),低于模型组(P<0.01)。结论 姜黄素可增强ox-LDL诱导损伤VE细胞的增殖、
迁移和侵袭能力,并抑制miR-21表达,具有改善血管内皮细胞功能。

Abstract:

Objective To study the biological mechanism of curcumin in controlling the expression of microRNA-21 (miR-21) and alleviating injury of vascular endothelial cells (VEC) induced by oxidized low density lipoprotein (ox-LDL). Methods VEC were divided into blank group, model group (treated with 100 μg/mL of ox-LDL) and curcumin group (treated with 100 μg/ml of ox-LDL+50 μg/ml of curcumin). The proliferation capacity of VEC was detected by using CCK-8 assay. The abilities of proliferation, migration and invasion of VEC were detected by using wound-healing test and Transwell assay. The mRNA and protein expressions of proliferating cell nuclear antigen (PCNA) and matrix metalloproteinase-9 (MMP-9) and miR-21 expression level were detected by using RT-qPCR and Western blotting assay in all groups. Results The survival rate decreased significantly in VEC treated with different concentrations of ox-LDL, and survival rate of VEC treated with 100 μg/mL of ox-LDL was (58.916±3.138) %, which was used for establishing the model of VEC injury. The VEC proliferation capacity (P<0.01), migration ability [(33.063±3.532) vs. (64.397±4.648), P<0.01] and invasion ability [(256.667±11.865) vs. (404.333±10.105)] were lower in model group than those in blank group (P<0.01). The VEC proliferation capacity (P<0.01), migration ability (61.773±2.451, P<0.01) and invasion ability [(393.000±11.547) were higher in curcumin group than those in model group (P<0.01). The mRNA and protein expressions of PCNA (P<0.01) and MMP-9 (P<0.01) were lower in model group than those in blank group. The mRNA and protein expressions of PCNA (P<0.01) and MMP-9 (P<0.01) were higher in curcumin group than those in model group. The relative expression of miR-21 was (8.020±0.483) in model group, which was higher than that in blank group (P<0.01). The relative expression of miR-21 was (2.241±0.205) in curcumin group, which was lower than that in model group (P<0.01). Conclusion Curcumin can enhance the abilities of proliferation, migration and invasion of injured VEC induced by ox-LDL, inhibit miR-21 expression and improve VEC function.

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  • 2008

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