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瑞舒伐他汀通过抑制 Akt、ERK1/2 和 GATA4 信号通路预防大鼠压力超负荷诱导的心肌肥厚。

Rosuvastatin prevents pressure overload‑induced myocardial hypertrophy via inactivation of the Akt, ERK1/2 and GATA4 signaling pathways in rats.

机构信息

Department of Health Care, Shandong Provincial Qianfoshan Hospital, Affiliated Hospital of Shandong University, Shandong University, Jinan, Shandong 250014, P.R. China.

出版信息

Mol Med Rep. 2013 Aug;8(2):385-92. doi: 10.3892/mmr.2013.1548. Epub 2013 Jun 25.

Abstract

Pressure overload‑induced myocardial hypertrophy is associated with a poor prognosis in humans and contributes to the development of cardiac arrhythmias, diastolic dysfunction and ultimate congestive heart failure. 3‑Hydroxy‑3‑methylglutaryl‑CoA (HMG‑CoA) reductase inhibitors, also known as statins, have been previously shown to induce regression of myocardial hypertrophy in aortic banding models. However, there is limited knowledge regarding the underlying molecular mechanisms. Therefore, we hypothesized that the myocardial hypertrophy‑related signaling pathways protein kinase B (Akt), extracellular signal‑regulated kinases 1 or 2 (ERK1/2) and GATA binding protein 4 (GATA4) activation pathways constitute targets of rosuvastatin (RSV). Therefore, the above‑mentioned activation pathways were hypothesized to be involved in the regression of pressure overload‑induced myocardial hypertrophy treated by RSV. Twenty‑eight Wistar rats were randomly allocated into 4 groups: the sham operation‑vehicle (SH‑V), abdominal aortic constriction‑vehicle (AAC‑V), abdominal aortic constriction‑RSV 10 mg/kg/day (AAC‑LO) and the abdominal aortic constriction‑RSV 20 mg/kg/day (AAC‑HI) group. Following the establishment of the abdominal aorta constriction model, we investigated the effect of RSV, a new hydrophilic statin, on abdominal aortic constriction‑induced myocardial hypertrophy as well as the underlying intercellular signaling pathways after 5 days and 4 weeks of drug intervention. Moreover, echocardiographic features and the left ventricular weight to final body weight ratio (LVW/BW) were determined. Cross‑sectional areas (CSAs) of cardiomyocytes were assessed by hematoxylin and eosin (H&E) staining. Atrial natriuretic factor (ANF), β‑myosin heavy chain (β‑MHC) and peroxisome proliferator‑activated receptor α (PPARα) messenger RNA (mRNA) expression was assessed using RT‑PCR. The phosphorylation of Akt, ERK1/2 and GATA4 were also examined using western blot analysis. Our results showed that RSV significantly attenuates pressure overload‑induced myocardial hypertrophy by preventing myocardial hypertrophy‑related activation of Akt, ERK1/2 and GATA4 signaling pathways.

摘要

压力超负荷诱导的心肌肥厚与人类不良预后相关,并导致心律失常、舒张功能障碍和充血性心力衰竭的发生。3-羟基-3-甲基戊二酰基辅酶 A(HMG-CoA)还原酶抑制剂,也称为他汀类药物,先前已被证明可在主动脉缩窄模型中诱导心肌肥厚的消退。然而,对于其潜在的分子机制知之甚少。因此,我们假设心肌肥厚相关信号通路蛋白激酶 B(Akt)、细胞外信号调节激酶 1 或 2(ERK1/2)和 GATA 结合蛋白 4(GATA4)激活途径是瑞舒伐他汀(RSV)的作用靶点。因此,我们假设上述激活途径参与了 RSV 治疗压力超负荷诱导的心肌肥厚的消退。28 只 Wistar 大鼠随机分为 4 组:假手术-载体(SH-V)、腹主动脉缩窄-载体(AAC-V)、腹主动脉缩窄-瑞舒伐他汀 10mg/kg/天(AAC-LO)和腹主动脉缩窄-瑞舒伐他汀 20mg/kg/天(AAC-HI)组。建立腹主动脉缩窄模型后,我们在 5 天和 4 周药物干预后,研究了新型亲水性他汀类药物瑞舒伐他汀对腹主动脉缩窄诱导的心肌肥厚以及细胞内信号通路的影响。此外,还测定了超声心动图特征和左心室重量与终体重比(LVW/BW)。通过苏木精和伊红(H&E)染色评估心肌细胞的横截面积(CSA)。通过逆转录聚合酶链反应(RT-PCR)评估心钠素(ANF)、β-肌球蛋白重链(β-MHC)和过氧化物酶体增殖物激活受体α(PPARα)信使 RNA(mRNA)的表达。通过 Western blot 分析还检测了 Akt、ERK1/2 和 GATA4 的磷酸化。我们的结果表明,RSV 通过阻止心肌肥厚相关的 Akt、ERK1/2 和 GATA4 信号通路的激活,显著减轻压力超负荷诱导的心肌肥厚。

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