中国临床康复
中國臨床康複
중국림상강복
CHINESE JOURNAL OF CLINICAL REHABILITATION
2005年
19期
254-256
,共3页
占成业%陶秀良%田橙%熊玮%郑智
佔成業%陶秀良%田橙%熊瑋%鄭智
점성업%도수량%전등%웅위%정지
高血压%肥大,左心室%细胞间粘附分子%巨噬细胞%丹参酮
高血壓%肥大,左心室%細胞間粘附分子%巨噬細胞%丹參酮
고혈압%비대,좌심실%세포간점부분자%거서세포%단삼동
背景:细胞间黏附分子1作为炎症反应的可靠标志物在动脉粥样硬化发病中具有重要的作用.近年来研究认为其介导的慢性炎症反应可能参与高血压左室肥厚的发病过程,但也有报道持相反观点.丹参酮ⅡA是丹参的一种脂溶性提取性,动物实验证明其具有抑制高血压左室肥厚发生的作用.目的:探讨细胞间黏附分子1在高血压左室肥厚发生中的作用及丹参酮ⅡA对其表达的影响.设计:随机对照观察.单位:华中科技大学同济医学院附属同济医院.材料:实验于2002-10/2004-01在华中科技大学同济医学院附属同济医院急诊科实验室完成,选用12周龄雄性WKY大鼠10只、自发性高血压SHR大鼠20只,分为对照组(WKY大鼠10只)、高血压组(SHR大鼠10只)、丹参酮ⅡA组(SHR大鼠10只).方法:丹参酮ⅡA组经尾静脉注射丹参酮ⅡA 1.5 mg/(kg·d)治疗,其他两组分别注射等量的蒸馏水.12周后断头处死所有大鼠留取心肌标本,应用苏木精-伊红染色、VG染色,免疫组化染色及心肌ED1标记检测心肌巨噬细胞浸润数,心肌细胞间黏附分子1 mRNA及蛋白的表达应用反转录-聚合酶链反应及酶链免疫吸附实验等方法.主要观察指标:各组大鼠心肌巨噬细胞浸润数,心肌细胞间黏附分子1mRNA及蛋白表达.结果:20只SHR和10只WKY大鼠被纳入实验,并全部进入结果分析,无脱失值.①与对照组比较,高血压组大鼠肥厚心肌中细胞间黏附分子1的mRNA及蛋白表达显著增加(0.176±0.087,0.537±0 195;0.104±0.011,0.173±0.027,P＜0.01或P＜0.05),巨噬细胞浸润明显(0.62±0.07,1.85±0.23,P＜0.01).②与高血压组比较,丹参酮ⅡA组大鼠心肌细胞间黏附分子1的mRNA及蛋白表达水平显著下调(0.537±0.195,0.291±0.106;0.173±0.027,0.125±0.014,P＜0.01或P＜0.05),巨噬细胞浸润数减少(1.85±0.23,1.16±0.17,P＜0.05),心肌细胞肥大和间质纤维化程度明显减轻.结论:心肌细胞间黏附分子1的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ⅡA抑制左室肥厚的效应可能与其下调细胞间黏附分子1表达,减少炎性细胞的心肌浸润有关.
揹景:細胞間黏附分子1作為炎癥反應的可靠標誌物在動脈粥樣硬化髮病中具有重要的作用.近年來研究認為其介導的慢性炎癥反應可能參與高血壓左室肥厚的髮病過程,但也有報道持相反觀點.丹參酮ⅡA是丹參的一種脂溶性提取性,動物實驗證明其具有抑製高血壓左室肥厚髮生的作用.目的:探討細胞間黏附分子1在高血壓左室肥厚髮生中的作用及丹參酮ⅡA對其錶達的影響.設計:隨機對照觀察.單位:華中科技大學同濟醫學院附屬同濟醫院.材料:實驗于2002-10/2004-01在華中科技大學同濟醫學院附屬同濟醫院急診科實驗室完成,選用12週齡雄性WKY大鼠10隻、自髮性高血壓SHR大鼠20隻,分為對照組(WKY大鼠10隻)、高血壓組(SHR大鼠10隻)、丹參酮ⅡA組(SHR大鼠10隻).方法:丹參酮ⅡA組經尾靜脈註射丹參酮ⅡA 1.5 mg/(kg·d)治療,其他兩組分彆註射等量的蒸餾水.12週後斷頭處死所有大鼠留取心肌標本,應用囌木精-伊紅染色、VG染色,免疫組化染色及心肌ED1標記檢測心肌巨噬細胞浸潤數,心肌細胞間黏附分子1 mRNA及蛋白的錶達應用反轉錄-聚閤酶鏈反應及酶鏈免疫吸附實驗等方法.主要觀察指標:各組大鼠心肌巨噬細胞浸潤數,心肌細胞間黏附分子1mRNA及蛋白錶達.結果:20隻SHR和10隻WKY大鼠被納入實驗,併全部進入結果分析,無脫失值.①與對照組比較,高血壓組大鼠肥厚心肌中細胞間黏附分子1的mRNA及蛋白錶達顯著增加(0.176±0.087,0.537±0 195;0.104±0.011,0.173±0.027,P＜0.01或P＜0.05),巨噬細胞浸潤明顯(0.62±0.07,1.85±0.23,P＜0.01).②與高血壓組比較,丹參酮ⅡA組大鼠心肌細胞間黏附分子1的mRNA及蛋白錶達水平顯著下調(0.537±0.195,0.291±0.106;0.173±0.027,0.125±0.014,P＜0.01或P＜0.05),巨噬細胞浸潤數減少(1.85±0.23,1.16±0.17,P＜0.05),心肌細胞肥大和間質纖維化程度明顯減輕.結論:心肌細胞間黏附分子1的過度錶達及其介導的炎性細胞浸潤在高血壓左室肥厚的髮病過程中具有重要作用.丹參酮ⅡA抑製左室肥厚的效應可能與其下調細胞間黏附分子1錶達,減少炎性細胞的心肌浸潤有關.
배경:세포간점부분자1작위염증반응적가고표지물재동맥죽양경화발병중구유중요적작용.근년래연구인위기개도적만성염증반응가능삼여고혈압좌실비후적발병과정,단야유보도지상반관점.단삼동ⅡA시단삼적일충지용성제취성,동물실험증명기구유억제고혈압좌실비후발생적작용.목적:탐토세포간점부분자1재고혈압좌실비후발생중적작용급단삼동ⅡA대기표체적영향.설계:수궤대조관찰.단위:화중과기대학동제의학원부속동제의원.재료:실험우2002-10/2004-01재화중과기대학동제의학원부속동제의원급진과실험실완성,선용12주령웅성WKY대서10지、자발성고혈압SHR대서20지,분위대조조(WKY대서10지)、고혈압조(SHR대서10지)、단삼동ⅡA조(SHR대서10지).방법:단삼동ⅡA조경미정맥주사단삼동ⅡA 1.5 mg/(kg·d)치료,기타량조분별주사등량적증류수.12주후단두처사소유대서류취심기표본,응용소목정-이홍염색、VG염색,면역조화염색급심기ED1표기검측심기거서세포침윤수,심기세포간점부분자1 mRNA급단백적표체응용반전록-취합매련반응급매련면역흡부실험등방법.주요관찰지표:각조대서심기거서세포침윤수,심기세포간점부분자1mRNA급단백표체.결과:20지SHR화10지WKY대서피납입실험,병전부진입결과분석,무탈실치.①여대조조비교,고혈압조대서비후심기중세포간점부분자1적mRNA급단백표체현저증가(0.176±0.087,0.537±0 195;0.104±0.011,0.173±0.027,P＜0.01혹P＜0.05),거서세포침윤명현(0.62±0.07,1.85±0.23,P＜0.01).②여고혈압조비교,단삼동ⅡA조대서심기세포간점부분자1적mRNA급단백표체수평현저하조(0.537±0.195,0.291±0.106;0.173±0.027,0.125±0.014,P＜0.01혹P＜0.05),거서세포침윤수감소(1.85±0.23,1.16±0.17,P＜0.05),심기세포비대화간질섬유화정도명현감경.결론:심기세포간점부분자1적과도표체급기개도적염성세포침윤재고혈압좌실비후적발병과정중구유중요작용.단삼동ⅡA억제좌실비후적효응가능여기하조세포간점부분자1표체,감소염성세포적심기침윤유관.
BACKGROUND: As a reliable marker of inflammation, intercellular adhesion molecule-1 (ICAM-1) plays an important role in atherogenesis. Recently, it is assumed in researches of recent years that chronic inflammation mediated by ICAM-1 is involved in hypertensive left ventricular hypertrophy probably, but there are still some objections reported. Tanshinone ⅡA is a kind of liposoluble extract from danshen(Radix Salviae Mitiorrhizae) . It is verified in animal experiment that it can inhibit hypertensive left ventricular hypertrophy.OBJECTIVE: To investigate the relationship between ICAM-1 and hypertensive left ventricular hypertrophy and the effect of tanshinone ⅡA on expression of ICAM-1.DESIGN:A randomized controlled observation was designed.SETTING: Tongji Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology.MATERIALS: The experiment was performed in the Laboratory of Emergency Department of Tongji Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology from October 2002 to January 2004. Ten male WKY rats(10 WKY rats) of 12-week-old and 20 rats with spontaneous hypertension(20 SHR rats) were employed and divided into the control group(10 WKY rats), hypertension group(10 SHR rats) and tanshinone ⅡA group(10 SHR rats).injected from caudal vein for treatment and distilled water at the same dose was injected in the other two groups. Twelve weeks later, the rats were sacrificed and myocardium was collected for specimen preparation. Haematoxylin and eosin(HE) staining, VG staining, immunocytochemical staining and myocardial ED1 labeling were applied to determine myocardial macrophage infiltration degree. The reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay(ELISA) were used to determine the expressions of ICAM-1 mRNA and protein.MAIN OUTCOME MEASURES: Degree of macrophages infiltration and the expressions of ICAM-1 mRNA and protein in myocardium in each group.RESULTS: Twelve SHR and 10 WKY rats were employed in the experiment pared with the control group, ICAM-1 mRNA and protein expressions in hypertrophic myocardium were increased significantly in hypertension group (0.176±0.087,0.537±0.195;0.104±0.011,0.173±0.027, P ＜0.01or P ＜ 0.05) . Infiltration of macrophage was significant(0. 62 ±0.07,non Ⅱ A group, the expressions of ICAM-1 mRNA and protein were decreased significantly(0. 537 ±0. 195, 0.291 ±0. 106; 0. 173 ±0.027, 0. 125± 0. 014, P ＜ 0.01 or P ＜ 0. 05); the amount of macrophages infiltration was decreased(1.85 ±0. 23, 1.16 ±0. 17, P ＜ 0.05) and the degree of cardiomyocytic hypertrophy and interstitial fibrosis was remarkably relieved.CONCLUSION: Excessive expression of myocardial ICAM-1 and its mediated inflammatory cellular infiltration plays an important role in hypertensive left ventricular hypertrophy. The inhibition of tanshinone ⅡA on left ventricular hypertrophy may be contributed to decreased expression of ICAM-1 and alleviated inflammatory cellular infiltration in myocardium.
