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目的探讨慢性缺氧心肌细胞β2-肾上腺素受体(β2-AR)表达的变化及其机制。方法成年雄性新西兰兔随机分成正常组、假手术组和紫绀组,其中紫绀组行肺动脉分支与左心耳侧侧吻合术,建立紫绀型心脏病动物模型。术后5周,监测动脉血氧分压(PO2)、动脉血氧饱和度(SaO2);Langendorff逆向灌注酶法分离心肌细胞,测定心肌细胞存活率;Western blot检测心肌细胞β2-AR、caspase-3、p-Akt蛋白表达水平。结果术后第5周,与正常组、假手术组相比,紫绀组PO2、SaO2显著降低,心肌细胞存活率显著下降,β2-AR、p-Akt蛋白表达明显低下,而caspase-3表达显著升高(分别P<0.01或<0.05)。结论兔紫绀型心脏病动物模型慢性缺氧心肌细胞β2-AR蛋白表达降低,可能是通过PI3K/Akt调节caspase-3的表达促进凋亡。
Objective To investigate the changes and mechanisms of β2-adrenergic receptor (β2-AR) expression in chronic hypoxic cardiomyocytes. Methods Adult male New Zealand white rabbits were randomly divided into normal group, sham operation group and cyanotic group. The cyanotic group and the lateral atrial appendage of cyanotic group were established in cyanotic group. Cardiac oxygenation (PO2) and arterial oxygen saturation (SaO2) were monitored at 5 weeks after operation. Cardiomyocytes were isolated by reverse perfusion Langendorff perfusion method. Cardiomyocytes survival rate was determined by Western blot. Β2-AR and caspase- 3, p-Akt protein expression levels. Results Compared with the normal group and the sham operation group, PO2 and SaO2 in cyanotic group decreased significantly at the 5th week after operation, while the survival rate of cardiomyocytes decreased significantly while the expression of β2-AR and p-Akt protein decreased significantly, while the expression of caspase-3 was significant (P <0.01 or <0.05, respectively). Conclusions The expression of β2-AR in hypoxic cardiomyocytes of rabbits with cyanotic heart disease is decreased, which may be due to the regulation of caspase-3 expression by PI3K / Akt.