Myocardial hypertrophy is a major pathological and physiological process during heart failure. Glucagon-like peptide 1 (GLP-1) is a glucagon incretin hormone released from the gut endocrine L-cells that has protective effects on various cardiovascular diseases, including hypertension, atherosclerosis, and myocardial hypertrophy. However, the protective mechanisms of GLP-1 in myocardial hypertrophy remain unclear. Here, we showed that the GLP-1 agonist liraglutide and dipeptidyl peptidase 4 inhibitor alogliptin decreased heart weight and cardiac muscle cell volume in spontaneously hypertensive rats (SHR). In H9C2 cell hypertensive models induced by angiotensin II, GLP-1 treatment reduced myocardial cell volume, inhibited the expressions of atrial natriuretic peptide, brain/B-type natriuretic peptide, β-myosin heavy chain, RhoA, and ROCK2, and decreased MLC and MYPT1 phosphorylation. When H9C2 cells were treated with H89, a PKA inhibitor, the inhibitory effect of GLP-1 disappeared, while the inhibitory role was enhanced under the treatment of Y-27632, a ROCK2 inhibitor. These results suggested that GLP-1 might reverse myocardial hypertrophy through the PKA/RhoA/ROCK2 signaling pathway.

中文翻译：

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胰高血糖素样肽1通过cAMP / PKA / RhoA / ROCK2信号逆转心肌肥大。

心肌肥大是心力衰竭期间的主要病理和生理过程。胰高血糖素样肽1（GLP-1）是从肠道内分泌L细胞释放的胰高血糖素肠降血糖素激素，对多种心血管疾病（包括高血压，动脉粥样硬化和心肌肥大）具有保护作用。但是，GLP-1在心肌肥大中的保护机制仍不清楚。在这里，我们显示了GLP-1激动剂利拉鲁肽和二肽基肽酶4抑制剂阿格列汀可降低自发性高血压大鼠（SHR）的体重和心肌细胞体积。在血管紧张素II诱导的H9C2细胞高血压模型中，GLP-1处理可减少心肌细胞体积，抑制心钠素，脑/ B型利钠肽，β-肌球蛋白重链，RhoA和ROCK2的表达，降低了MLC和MYPT1的磷酸化。当用PKA抑制剂H89处理H9C2细胞时，GLP-1的抑制作用消失了，而在ROCK2抑制剂Y-27632的作用下，其抑制作用增强了。这些结果表明，GLP-1可能通过PKA / RhoA / ROCK2信号通路逆转心肌肥大。