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目的:观察GHRP-6对心力衰竭模型大鼠心脏功能的调节作用和其对PI3K/Akt/Caspase-9信号转导通路的影响。方法:建立GHRP-6对心力衰竭模型大鼠心肌细胞的保护模型,比较PI3K p110α、Akt p-Thr308和Akt p-Ser473在正常对照组、假手术组和模型组大鼠心肌细胞左心室后壁和室间隔心肌细胞内的表达。流式细胞术(FCM)检测模型组与正常对照组和假手术组大鼠心肌细胞的凋亡率。结果:在大鼠心肌细胞左心室后壁和室间隔心肌细胞内,模型组大鼠心肌细胞的PI3K p110α、Akt p-Thr308和Akt p-Ser473阳性表达量较正常对照组和假手术组显著降低(P<0.05);与正常对照组、假手术组和模型组大鼠心肌细胞的分别比较,GHRP-6治疗组大鼠心肌细胞的阳性表达量显著升高(P<0.05)。模型组大鼠心肌细胞的Caspase-9和Caspase-3阳性表达量较正常对照组和假手术组显著增高(P<0.05);与正常对照组、假手术组和模型组分别比较,GHRP-6治疗组阳性表达量显著降低(P<0.05)。FCM结果显示,模型组大鼠心肌细胞与正常对照组和假手术组比较,凋亡率显著升高(P<0.05);GHRP-6治疗组与模型组比较,凋亡率明显降低(P<0.05)。相关程度分析显示,PI3K p110α与Akt p-Thr308、p-Ser473蛋白阳性表达量均呈中度正相关;Akt p-Thr308、p-Ser473与Caspase-9蛋白阳性表达量均呈中度负相关;Caspase-9与Caspase-3蛋白阳性表达量呈高度正相关。结论:GHRP-6通过调控PI3K/Akt/Caspase-9/Caspase-3信号转导通路,抑制心力衰竭模型大鼠心肌细胞凋亡,是其实现心肌细胞保护作用机制之一。
AIM: To observe the regulatory effect of GHRP-6 on cardiac function in heart failure model rats and its effect on PI3K / Akt / Caspase-9 signal transduction pathway. Methods: The protective model of GHRP-6 was established in cardiomyocytes of heart failure model rats. The expressions of PI3K p110α, Akt p-Thr308 and Akt p-Ser473 in normal control group, sham operation group and model group And ventricular septal cardiomyocytes. Flow cytometry (FCM) was used to detect the apoptosis rate of cardiomyocytes in model group, normal control group and sham operation group. Results: The positive expression of PI3K p110α, Akt p-Thr308 and Akt p-Ser473 in myocardial cells of left ventricle and interventricular septal myocardium of rats in model group were significantly lower than those in normal control group and sham operation group P <0.05). Compared with normal control group, sham operation group and model group, the positive expression of cardiomyocytes in GHRP-6 treatment group was significantly increased (P <0.05). The positive expression of Caspase-9 and Caspase-3 in myocardial cells in model group was significantly higher than that in normal control group and sham operation group (P <0.05). Compared with normal control group, sham operation group and model group, GHRP-6 The positive expression of the treatment group was significantly lower (P <0.05). The results of FCM showed that the apoptotic rate of myocardial cells in model group was significantly higher than that in normal control group and sham operation group (P <0.05), and the apoptosis rate in GHRP-6 treated group was significantly lower than that in model group (P < 0.05). Correlation analysis showed that there was a moderate positive correlation between PI3K p110α and Akt p-Thr308 and p-Ser473 protein expression, and negative correlation between Akt p-Thr308, p-Ser473 and Caspase-9 protein expression; Caspase-9 and Caspase-3 protein expression was positively correlated. CONCLUSION: GHRP-6 inhibits cardiomyocyte apoptosis in heart failure model rats by regulating the PI3K / Akt / Caspase-9 / Caspase-3 signal transduction pathway, which is one of the mechanisms of cardiomyocyte protective effect.