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目的:观察阿托伐他汀对大鼠甲状旁腺素1-34(rPTH1-34)诱导的新生大鼠心室肌细胞肥大的抑制作用及丝裂素活化蛋白激酶激酶1/细胞外信号调节激酶1/2(MKK1/ERK1/2)表达的变化,分析阿托伐他汀抑制心肌肥大的可能机制。方法:以原代培养的新生Wsitar大鼠心室肌细胞为研究对象,3H-亮氨酸掺入率检测细胞蛋白合成速率,BCA法测定单个细胞蛋白含量,RT-PCR检测心房利钠尿肽mRNA(ANPmRNA)的表达,Western blot方法测定p-MKK1、p-ERK1/2蛋白的表达。结果:1.10-7mmol/LrPTH1-34孵育24h可增加体外培养的心肌细胞蛋白合成速率和ANPmRNA表达,使p-MKK1及p-ERK1/2蛋白表达升高(P<0.05)。2.10-5mmol/L阿托伐他汀能抑制心肌细胞蛋白合成速率及单细胞蛋白含量的增加(P<0.05),且对正常心肌细胞没有影响(P>0.05)。3.10-5mmol/L阿托伐他汀能抑制p-MKK1、p-ERK1/2的表达(P<0.05)。结论:阿托伐他汀能抑制PTH诱导的心肌细胞肥大的发生,可能与抑制MKK1/ERK1/2的活性有关。
AIM: To observe the inhibitory effect of atorvastatin on ventricular myocyte hypertrophy induced by parathyroid hormone 1-34 (rPTH1-34) and the effects of mitogen-activated protein kinase kinase 1 / extracellular signal-regulated kinase 1 / 2 (MKK1 / ERK1 / 2) expression changes, analysis of atorvastatin possible mechanism of inhibiting cardiac hypertrophy. Methods: Primary cultured ventricular myocytes of Wsitar rats were studied. 3H-leucine incorporation rate was used to detect the rate of cellular protein synthesis. Single cell protein content was measured by BCA method. Atrial natriuretic peptide (ANPmRNA) expression, Western blot method was used to determine the expression of p-MKK1, p-ERK1 / 2 protein. Results: After incubated with10-7mmol / LrPTH1-34 for24h, the protein synthesis rate and the expression of ANP mRNA in cardiomyocytes were increased and the expressions of p-MKK1 and p-ERK1 / 2 were increased (P <0.05). 2.10-5mmol / L atorvastatin can inhibit the rate of myocardial cell protein synthesis and single cell protein content (P <0.05), and had no effect on normal cardiomyocytes (P> 0.05). 3.10-5mmol / L atorvastatin can inhibit the expression of p-MKK1, p-ERK1 / 2 (P <0.05). Conclusions Atorvastatin can inhibit PTH-induced cardiomyocyte hypertrophy and may be related to the inhibition of MKK1 / ERK1 / 2 activity.