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目的观察丹参酮ⅡA磺酸钠盐对腹主动脉缩窄致高血压大鼠肥厚心肌血管紧张素Ⅱ受体(AT1R)基因、蛋白表达以及对STAT3蛋白表达的影响,探讨其延缓心肌肥厚的机制。方法取24只9周龄SD大鼠,环扎其腹主动脉,制成高血压大鼠模型,随机分为模型组(n=8)、丹参酮ⅡA磺酸钠组(n=8)、缬沙坦组(n=8);另取8只行假手术,作为假手术组。给药8周后测量大鼠的尾动脉收缩压(SBP)及左室质量指数(LVMI),应用HE染色、VG染色,检测心肌纤维直径(MFD),采用RT-PCR、Western blotting方法分别检测AT1R的mRNA和蛋白的表达水平以及STAT3蛋白的表达水平。结果与假手术组比较,模型组的SBP、LVMI、MFD均显著增加;AT1R mRNA和蛋白的表达水平明显增高,STAT3的表达也明显升高(P<0.05)。与模型组相比,丹参酮ⅡA磺酸钠组大鼠LVMI、MFD均显著降低;AT1RmRNA、蛋白表达和STAT3的表达均受到一定程度的抑制,但作用不如缬沙坦明显(P<0.05)。结论丹参酮ⅡA磺酸钠有延缓心肌肥厚的作用,可能与一定程度上抑制AT1R以及STAT3的表达有关。
Objective To observe the effects of sodium tanshinone IIA sulfonate on the expression of angiotensin II receptor (AT1R) gene and protein and the expression of STAT3 protein in hypertrophic heart in hypertensive rats with abdominal aortic coarctation, and to explore its mechanism of delaying myocardial hypertrophy. Methods Twenty-four 9-week-old Sprague-Dawley rats were circumcised and the abdominal aorta was ligated to obtain a model of hypertensive rats. The rats were randomly divided into model group (n=8), tanshinone IIA sodium sulfonate group (n=8), and sputum. Satan group (n=8); another 8 patients underwent sham surgery as a sham group. After 8 weeks of dosing, the tail artery systolic pressure (SBP) and left ventricular mass index (LVMI) were measured. HE staining and VG staining were used to detect myocardial fiber diameter (MFD). RT-PCR and Western blotting methods were used to detect the blood pressure. AT1R mRNA and protein expression levels and STAT3 protein expression levels. Results Compared with the sham group, the SBP, LVMI and MFD of the model group increased significantly; AT1R mRNA and protein expression levels increased significantly, and STAT3 expression also increased significantly (P<0.05). Compared with the model group, LVMI and MFD of rats in the tanshinone IIA sodium sulphonate group were significantly decreased; AT1R mRNA and protein expression and STAT3 expression were inhibited to some extent, but the effect was not as obvious as valsartan (P<0.05). Conclusion Sodium tanshinone II A sulfonate can delay myocardial hypertrophy and may be related to inhibiting the expression of AT1R and STAT3 to some extent.