细胞间黏附分子-1在高血压左室肥厚发病中的作用及丹参酮ⅡA对其表达的影响  

Relationship between intercellular adhesion molecule-1 and hypertensive left ventricular hypertrophy and the effect of tanshinoneⅡA on expression of intercellular adhesion molecule-1

作　　者：占成业[1] 陶秀良[2] 田橙[1] 熊玮[1] 郑智[1] 

机构地区：[1]华中科技大学同济医学院附属同济医院急诊科,湖北武汉430030 [2]华中科技大学同济医学院附属同济医院中西医结合研究所,湖北武汉430030

出　　处：《中国中西医结合急救杂志》2004年第4期208-211,F003,共5页Chinese Journal of Integrated Traditional and Western Medicine in Intensive and Critical Care

基　　金：湖北省自然科学基金资助项目(2000J064)

摘　　要：目的 :探讨细胞间黏附分子- 1(ICAM-1)在高血压左室肥厚发生中的作用及丹参酮 A对其表达的影响。方法 :12周龄雄性 Wistar-Kyoto(WKY)大鼠和自发性高血压大鼠 (SHR)共 30只 ,随机分为对照组、高血压组、丹参酮 ⅡA组。丹参酮 Ⅱ A组经尾静脉连续注射丹参酮 Ⅱ A治疗 12周。断头处死大鼠后留取心肌标本 ,进行苏木素伊红 (HE)、范吉逊 (VG)染色 ,观察心肌细胞形态和胶原分布情况 ;免疫组化染色及 ED1标记显示心肌巨噬细胞浸润 ;逆转录聚合酶链反应检测心肌 ICAM -1m RNA表达 ;酶联免疫吸附试验(EL ISA)检测 ICAM -1的蛋白表达。结果 :与对照组 WKY大鼠比较 ,SHR组肥厚心肌中 ICAM-1的 m RNA及蛋白表达均显著增加 (P<0 .0 1和 P<0 .0 5 ) ,巨噬细胞浸润明显 (P<0 .0 1)。应用丹参酮 A治疗后 ,SHR组的心肌 ICAM-1的 m RNA及蛋白表达水平均显著下调 (P<0 .0 1和 P<0 .0 5 ) ,巨噬细胞浸润数减少(P<0 .0 5 ) ,心肌细胞肥大和间质纤维化程度明显减轻。结论 :心肌 ICAM-1过度表达及其介导的炎性细胞浸润在高血压左室肥厚的发病过程中具有重要作用 ;丹参酮 A抑制左室肥厚的效应可能与其下调 ICAM-1表达 ,减少炎性细胞的心肌浸润有关。Objective: To investigate the relationship between intercellular adhesion molecule-1((ICAM-1)) and hypertensive left ventricular hypertrophy and the effect of tanshinoneⅡA on expression of (ICAM-1). Methods: Thirty male 12-week-old spontaneously hypertensive rats(SHR) and Wistar-Kyoto(WKY) rats were randomly divided into three groups: control group, hypertensive group, and tanshinoneⅡA group. Animals in tanshinoneⅡA groups injected tanshinoneⅡA by cauda vein for 12 weeks. Cardiomyocyte morphosis and collagen distribution were observed with hematoxylin and eosin(HE) and van Gieson(VG) staining. The degree of macrophages infiltration was examined with immunocytochemical staining and ED1 (labelling), and the expression of ICAM-1 mRNA and protein in myocardia was measured with reverse (transcription-polymerase) chain reaction(RT-PCR) and enzyme-linked immunosorbent assay(ELISA), (respectively). Results: Compared with WKY rats, SHR exhibited higher level of ICAM-1 mRNA and protein expression(P<0.01 or P<0.05) and the amount of macrophages infiltration(P<0.01) in hypertrophic (myocardia). After treatment with tanshinoneⅡA, the expression of ICAM-1 and the amount of macrophages in myocardia of SHR greatly decreased(P<0.01 or P<0.05), and the degree of cardiomyocyte hypertrophy and interstitial fibrosis was significantly relieved. Conclusion: The macrophages infiltration caused by (excessive) (expression) of myocardial ICAM-1 plays an important role in hypertensive left ventricular (hypertrophy), and the inhibition of tanshinoneⅡA on left ventricular (hypertrophy) may be contributed to (decrease) in (ICAM-1) expression and macrophages infiltration in myocardia.

关 键 词：细胞间黏附分子-1 左室肥厚 高血压 巨噬细胞浸润 丹参酮ⅡA 

分 类 号：R285[医药卫生—中药学]