【摘要】 目的：研究灯盏花素对自发性高血压大鼠(SHR)心肌细胞凋亡和心室重塑的作用和机制。方法：将18只10月龄伴有左心室肥厚的SHR 随机分为灯盏花素组、福辛普利组和生理盐水(对照)组进行为期8周的干预治疗，观察其对SHR收缩压、心率、左心室重量/体重指数、心肌细胞超微结构、心肌细胞凋亡、Bax和Bcl-2基因蛋白表达和心肌细胞蛋白激酶C(PKC)活性的影响。结果：灯盏花素和福辛普利均能显著降低左心室重量/体重指数(P均<0.01)、改善心肌细胞超微结构、降低心肌细胞Bcl-2基因蛋白表达和心肌细胞膜PKC活性(P均<0.01)、增加心肌细胞Bax基因蛋白表达和促进心肌细胞凋亡(P均<0.01)。福辛普利还能显著降低SHR的收缩压(P均<0.01)。结论：灯盏花素和福辛普利均能显著逆转SHR的心室重塑，具有心脏保护作用，上调细胞凋亡诱导基因(Bax基因)表达和下调细胞凋亡抑制基因(Bcl-2基因)表达及抑制心肌细胞膜PKC活性，从而促进心肌细胞凋亡是其可能的机制之一。更多还原

【Abstract】 Objective: To study the effects and mechanisms of protein kinase C(PKC) inhibitor(scutellarein) on cardiomyocyte apoptosis and ventricular remodeling in spontaneously hypertensive rats (SHR). Methods: 18 SHRs with left ventricular hypertrophy(LVH) aged 10 months were randomly divided into 3 groups and treated for 8 weeks with scutellarein, fosinopril and 0.9% sodium chloride solution(control) respectively.The effects of above drugs on systolic blood pressure (SBP), heart rate (HR), left ventricular hypertrophic index (left ventricular weight/body weight,LVW/BW), cardiocyte ultramicrostructure, cardiac myocyte apoptosis, apoptosis-associated gene (Bax and Bcl-2 gene) protein expression and PKC activity were observed. Results: Compared with control group, scutellarein and fosinopril could significantly reduce left ventricular hypertrophic index(all P values less than 0.01), ameliorate ultramicrostructure of cardiac hypertrophy, suppress Bcl-2 protein expression (all P values less than 0.01), lower the membrane PKC (PKCm) activity(all P values less than 0.01), stimulate Bax protein expression and promote cardiomyocyte apoptosis of SHRs with left ventricular hypertrophy (all P values less than 0.01). Fosinopril could remarkably decrease systolic blood pressure (all P values less than 0.01) but did not affect heart rate of SHRs with left ventricular hypertrophy (all P values more than 0.05). Scutellarein could not influence systolic blood pressure and heart rate of SHRs with left ventricular hypertrophy (all P values more than 0.05). Conclusion: Scutellarein and fosinopril can significantly reverse ventricular remodeling of SHR and preserve cardiac muscle. The mechanisms of their above-mentioned effects may be related to increase of cardiac myocyte apoptosis triggered by them via upregulation of apoptosis induced gene(Bax gene) expression and downregulation of apoptosis suppressor gene(Bcl-2 gene) expression as well as suppression of PKC activity.更多还原