丹参酮ⅡA对猪主动脉内皮细胞受血管紧张素Ⅱ作用时产生NO及eNOS基因表达的影响

Effect of Tanshinone ⅡA on Angiotensin Ⅱ Induced Nitric Oxide Production and Endothelial Nitric Oxide Synthase Gene Expression in Cultured Porcine Aortic Endothelial Cells

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中文关键词: 丹参酮ⅡA 血管紧张素Ⅱ 内皮型一氧化氮合酶内皮细胞基因表达

英文关键词:Tanshinone ⅡA angiotensin Ⅱ endothelial nitric oxide synthase endothelial cell gene expression

基金项目:国家自然科学基金资助项目(No.30500657)

作者	单位
李永胜	华中科技大学同济医学院附属同济医院急诊科 (武汉430030)
梁黔生	华中科技大学同济医学院附属同济医院急诊科 (武汉430030)
王进	华中科技大学同济医学院附属同济医院急诊科 (武汉430030)
王照华	华中科技大学同济医学院附属同济医院急诊科 (武汉430030)
杨光田	华中科技大学同济医学院附属同济医院急诊科 (武汉430030)
郑智	华中科技大学同济医学院附属同济医院急诊科 (武汉430030)

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中文摘要:

目的探讨丹参酮ⅡA对血管内皮细胞的保护作用。方法采用硝酸还原酶法、逆转录聚合酶链式反应(RT-PCR)和免疫组织化学法,分别检测不同作用时间(1h、6h、24h)的血管紧张素Ⅱ(AngⅡ)以及在AngⅡ作用的不同时间点(0h点为A组、6h点为B组)加入丹参酮ⅡA对培养的猪主动脉内皮细胞产生NO及其内皮型一氧化氮合酶(eNOS)的蛋白和mRNA表达。结果(1)随着AngⅡ作用时间的延长,血管内皮细胞NO的产生及eNOS的表达呈显著下降(P<0.01),表现出时间依赖性的负性作用。(2)丹参酮ⅡA可抑制AngⅡ对内皮细胞分泌NO及eNOS基因表达的负性作用(P<0.01)。(3)在丹参酮ⅡA作用1h、6h,A组的抑制效应明显强于B组(P<0.05);随着作用时间延长至24h,两组比较差异无显著性。结论丹参酮ⅡA可抑制AngⅡ对血管内皮细胞分泌NO以及细胞eNOS基因表达的负性作用。

英文摘要:

Objective To investigate the protective effect of tanshinone ⅡA on porcine aortic endothelial cells(PAEC).Methods PAEC were stimulated with angiotensin Ⅱ(Ang-Ⅱ)for different acting time(1 h,6 h and 24 h)and Tanshinone ⅡA was added along with Ang-Ⅱ stimulation(Group A)or 6 h after it(Group B).The nitric oxide(NO)level,the protein and mRNA expression of nitric oxide synthase(eNOS)in PAEC were measured by nitric acid deoxidizing assay,RT-PCR and immunohistochemical assay,respectively.Results With the prolongation of acting time of Ang-Ⅱ,the level of NO and eNOS expression in PAEC sequentially decreased in a negative acting time dependent manner(P<0.01),which could be inhibited by tanshinone ⅡA treatment independent to the dosage used(P<0.01).The inhibitory effect of tanshinone ⅡA was better in Group A than that in Group B either at 1 h or at 6 h after treatment(P<0.05).However,24 h later,no significant difference was found between the effect in the two groups(P>0.05).Conclusion Tanshinone ⅡA could inhibit the negative effect of Ang-Ⅱ on NO production and eNOS expression in PAEC.

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