丹参酮ⅡA对内皮细胞环氧合酶2表达的影响及相关机制  被引量:8

Effect of Tanshinone Ⅱ A on Endothelial Cells' Cyclooxygenase-2 Expression and the Relative Mechanisms

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作  者:王红艳[1] 蔡凡[1] 徐春亮[2] 曹久妹[1] 陈晓南[1] 吴方[1] 

机构地区:[1]上海交通大学医学院附属瑞金医院老年病科 [2]上海交通大学医学院中国科学院上海生命科学研究院健康科学研究中心,上海市200025

出  处:《中国动脉硬化杂志》2014年第10期997-1000,共4页Chinese Journal of Arteriosclerosis

基  金:上海市科委基金资助(124119a6800);上海市公共卫生重点学科建设计划项目(12GWEX1002)

摘  要:目的探讨丹参酮ⅡA对主动脉内皮细胞环氧合酶2(COX-2)表达的影响及相关机制。方法体外培养人主动脉内皮细胞株并分为三组:血管紧张素Ⅱ(100 nmol/L)组、血管紧张素Ⅱ(100 nmol/L)+丹参酮ⅡA(1μmmol/L)组及对照组,共培养10 min、1 h及2 h后分别收集细胞,运用实时荧光定量PCR检测COX-2 mRNA的表达量,Western blot检测COX-2、p38丝裂原活化蛋白激酶(p38MAPK)、磷酸化p38MAPK(p-p38MAPK)、核因子κB(NF-κB)及磷酸化NF-κB(p-NF-κB)蛋白表达的变化。结果在血管紧张素Ⅱ的作用下,内皮细胞内COX-2 mRNA和蛋白表达水平明显增加(P<0.01),且p-p38MAPK和p-NF-κB水平也同步提高(P<0.01)。加用丹参酮ⅡA处理后,内皮细胞COX-2 mRNA和蛋白表达水平显著下降(P<0.01),p-p38MAPK和p-NF-κB水平也受到明显抑制(P<0.01)。结论丹参酮ⅡA明显抑制主动脉内皮细胞COX-2的表达,其机制可能与抑制p38MAPK、NF-κB的磷酸化有关。Aim To investigate the effect of Tanshinone ⅡA on endothelial cells’ cyclooxygenase-2( COX-2)expression and the relative mechanisms. Methods Human aortic endothelial cells were incubated in vitro and then co-cultured with angiotension Ⅱ( 100 nmol / L),Tanshinone ⅡA( 1 μmmol / L) and no drugs respectively for 10 minutes,1 hour and 2 hours. The expressions of COX-2 mRNA were measured by real time-PCR and COX-2,p38 MAPK,pp38MAPK,NF-κB and p-NF-κB protein levels were measured by Western blot assay. Results AngiotensionⅡ could induce the expression of COX-2 mRNA and protein( P 〈 0. 01) as the same as the phosphorylation of p38 MAPK and NF-κB( P 〈 0. 01). Incubating human aortic endothelial cells with angiotensionⅡ and Tanshinone ⅡA suppressed the expression of COX-2( P 〈 0. 01) and the phosphorylation of p38 MAPK and NF-κB was also decreased( P 〈 0. 01).Conclusion Tanshinone ⅡA could suppress the expression of COX-2 and it may be achieved through inhibiting the phosphorylation of p38 MAPK and NF-κB.

关 键 词:丹参酮ⅡA 环氧合酶2 血管紧张素Ⅱ P38丝裂原活化蛋白激酶 核因子ΚB 

分 类 号:R96[医药卫生—药理学]

 

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