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目的:观察压力负荷增加大鼠心肌组织结缔组织生长因子(Connective Tissue Growth Factor,CTGF)表达的改变,探讨丹参酮ⅡA(TanshinoneⅡA,TanⅡA)对心肌纤维化的保护作用。方法:采用腹主动脉缩窄术制备压力负荷增加心肌纤维化模型,随机分成4组(n=8),假手术组(Sham组)、模型组(Model组)、丹参酮ⅡA组[TanⅡA组,20 mg/(kg·d)]及阳性对照药物卡托普利组[Captopril组,100 mg/(kg·d)]。术后4周成功造模并开始给药,疗程为4周。8周后检测心室质量指数、左心室重量指数、心肌组织病理学、心肌羟脯氨酸含量以及心肌组织CTGF蛋白含量。结果:①与Sham组比较,Model组大鼠心脏质量指数和左心脏质量指数明显升高(P<0.01);与Model组比较,TanⅡA组则显著降低(P<0.01)。②与Sham组比较,Model组大鼠心肌羟脯氨酸含量明显升高(P<0.01);与Model组比较,TanⅡA组则显著降低(P<0.01)。③与Sham组比较,Model组大鼠心肌组织CTGF表达显著升高(P<0.01);与Model组比较,TanⅡA组则显著降低(P<0.01)。结论:TanⅡA组能抑制心肌肥厚,减轻心肌纤维化,此作用可能与下调心肌局部CTGF水平有关。
OBJECTIVE: To observe the changes of connective tissue growth factor (Connexin Tissue Growth Factor, CTGF) expression induced by pressure overload in rats and to explore the protective effect of TanshinoneⅡA (TanⅡA) on myocardial fibrosis. Methods: A model of myocardial fibrosis was established by abdominal aortic constriction. The rats were randomly divided into 4 groups (n = 8), Sham group, Model group, Tan ⅡA group, 20 mg / (kg · d)] and the positive control captopril group [Captopril group, 100 mg / (kg · d)]. After 4 weeks of successful modeling and start the medication, the course of treatment for 4 weeks. After 8 weeks, the ventricular mass index, left ventricular mass index, myocardial histopathology, hydroxyproline content and myocardial CTGF protein content were detected. Results: ①Compared with Sham group, the heart mass index and left heart mass index of Model group were significantly increased (P <0.01); Compared with Model group, TanⅡA group was significantly lower (P <0.01). ②Compared with Sham group, the content of hydroxyproline in myocardium of Model group was significantly increased (P <0.01); Compared with Model group, TanⅡA group was significantly reduced (P <0.01). ③Compared with Sham group, the expression of CTGF in myocardium of Model group was significantly increased (P <0.01); Compared with Model group, TanⅡA group was significantly lower (P <0.01). Conclusion: Tan Ⅱ A group can inhibit cardiac hypertrophy and reduce myocardial fibrosis, which may be related to downregulation of myocardial CTGF.