目的:观察丹参酮ⅡA对压力超负荷大鼠心室重构时血红素加氧酶-1(Hemeoxygenase-1,HO-1)蛋白及mRNA基因表达的影响。方法:40只SD大鼠随机编号,抽取8只为假手术组,其余32只大鼠采用腹主动脉缩窄术制备压力超负荷模型。术后存活22只大鼠再随机分成3组,分别为模型组(n=7)、丹参酮ⅡA组(n=7)及丹参酮ⅡA+HO-1抑制剂锌原卟啉组(n=8),术后4周开始给药,给药4周后检测心室质量指数(heart weight index,HWI)、左心室质量指数(left ventricular weight index,LVWI)、心肌组织病理学(HE染色)以及心肌组织的HO-1蛋白和mRNA基因表达水平。结果:1与假手术组比较,模型组大鼠HWI和LVWI明显升高(P〈0.01);与模型组比较,丹参酮ⅡA组和丹参酮ⅡA+锌原卟啉组的HWI和LVWI均有不同程度的下降,而丹参酮ⅡA组改善更为显著(P〈0.01)。2HE染色结果显示,与假手术组比较,模型组大鼠心肌纤维化程度加重;与模型组相比,丹参酮ⅡA组和丹参酮ⅡA+锌原卟啉组组心肌组织形态学均有不同程度的改善,丹参酮ⅡA组改善更为明显。3丹参酮ⅡA组大鼠的HO-1蛋白和mRNA基因表达水平均明显高于其他3组,且差异有统计学意义(均P〈0.01)。结论:丹参酮ⅡA能减轻心肌纤维化,抑制心室重构进程,此作用可能与丹参酮ⅡA诱导HO-1表达上调有关。
Objective :To obeserve the effect of Tanshinone IIA on the expression of Hemeoxygenase-1 protein and mRNA in ven- tricular remodeling in rats with overloaded pressure. Methods : 8 in 40 SD rats were randomly selected as control group ( Sham group), with the remaining 32 rats were prepared with abdominal aortic coaretation operation to establish model rats under overloa- ded pressure. 22 survival rats after operation were randomly divided into three groups, namely, Model group ( n = 7 ), Tan IIA group ( n = 7) and TanlIA + HO-1 inhibitor treatment group ( Tan IIA + ZnPP group, n = 8 ). After eight weeks of treatment, the heart weight index,left ventrieular weight index, HE staining and the expression level of HO-1 protein and mRNA were detected. Re- suits : ①Compared with those of the Sham group, the cardiac mass index and left ventrieular mass index of the Model group signifi- candy increased (P 〈 0.01 ). Compared with that of the Model group, these indexes significantly decreased in Tan IIA group (P 〈 0.01 ). ② It is shown with HE staining that compared with that of the Sham group,the extent of myocardial fibrosis of the Model group was seriously aggravated. Compared with that of the Model group, the tissue morphology of both the Tan IIA group and theTan IIA + ZnPP group got improved by different degrees,with that of the Tan IIA group improving more significantly. ③ The HO- 1 protein and mRNA expression levels of the Tan IIA group were significantly higher than those of other three groups respectively (P 〈 0.01 ). Conclusion:Tan IIA can attenuate myocardial fibrosis and inhibit ventricular remodeling,which may be related to the upregulation of HO-I expression.