论文部分内容阅读
目的观察康心饮对缺血性心肌病(ICM)大鼠心肌凋亡及PI3K/Akt/FoxO1信号通路的影响,探讨其对ICM的作用及可能机制。方法 66只大鼠按随机数字表法分为假手术组、模型组、卡托普利组及康心饮低、中、高剂量组,每组11只。采用左前降支结扎法制备缺血性心肌病模型。模型组予生理盐水10 m L/(kg·d)早晚灌胃,卡托普利组予卡托普利2.86 mg/(kg·d)早晚灌胃,康心饮低、中、高组分别予康心饮9.2、18.4、36.8 g/(kg·d)早晚灌胃,给药2周。TUNEL法检测心肌凋亡情况,Western blot检测Bcl-2、Bax、Caspase-3、PI3K、Akt、FoxO1蛋白表达,RT-PCR检测PI3K、Akt、FoxO1 mRNA表达。结果与假手术组比较,模型组心肌凋亡增多(P<0.05),Bax、Caspase-3蛋白表达量升高(P<0.05,P<0.01),Bcl-2蛋白表达量下降(P<0.01),PI3K、p-Akt、p-FoxO1蛋白和PI3K、Akt、FoxO1 mRNA表达均下降(P<0.05);与模型组比较,康心饮组低、中、高剂量和卡托普利组心肌凋亡均明显减少(P<0.01),Bax和Caspase-3蛋白表达下降,Bcl-2蛋白表达增加(均P<0.05),PI3K、p-Akt、p-FoxO1蛋白及PI3K、Akt、FoxO1 mRNA表达均升高(P<0.01),且康心饮高剂量组和卡托普利组优于康心饮低、中剂量组(P<0.05)。结论康心饮可能通过激活PI3K/Akt/FoxO1信号通路,抑制ICM心肌细胞凋亡。
Objective To observe the effects of Kangxin Yin on myocardial apoptosis and PI3K / Akt / FoxO1 signal pathway in rats with ischemic cardiomyopathy (ICM) and explore the possible mechanism of Kangxin Yin on ICM. Methods Sixty-six rats were randomly divided into sham operation group, model group, captopril group and Kangxin Yin low, medium and high dose group, 11 rats in each group. Ischemic cardiomyopathy model was made by left anterior descending branch ligation. The rats in the model group were treated with saline 10 m L / (kg · d) orally in the morning and evening, captopril was given to captopril 2.86 mg / (kg · d) Healthy heart drink 9.2,18.4,36.8 g / (kg · d), gavage for 2 weeks. The apoptosis of myocardium was detected by TUNEL method. The expressions of Bcl-2, Bax, Caspase-3, PI3K, Akt and FoxO1 were detected by Western blot. The expressions of PI3K, Akt and FoxO1 mRNA were detected by RT-PCR. Results Compared with the sham operation group, the apoptosis of model group increased (P <0.05), the expression of Bax and Caspase-3 protein increased (P <0.05, P <0.01) and the expression of Bcl- ), PI3K, p-Akt, p-FoxO1 protein and PI3K, Akt, FoxO1 mRNA expression decreased; compared with the model group, Kang Xin Yin group low, medium and high dose and captopril group myocardial (P <0.01), decreased the expression of Bax and Caspase-3 protein, increased the expression of Bcl-2 protein (all P <0.05), PI3K, p-Akt and p-FoxO1 protein and PI3K, Akt and FoxO1 mRNA (P <0.01), and Kangxin Yin high-dose group and captopril group was better than Kangxin Yin low dose group (P <0.05). Conclusion Kangxin Yin may inhibit the apoptosis of ICM cardiomyocytes by activating PI3K / Akt / FoxO1 signaling pathway.