Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, 563000, China; The First People's Hospital of Zunyi, Zunyi, Guizhou, 563006, China.
Key Laboratory of Basic Pharmacology of Ministry of Education and Joint International Research Laboratory of Ethnomedicine of Ministry of Education, Zunyi Medical University, Zunyi, Guizhou, 563000, China.
Biomed Pharmacother. 2019 Apr;112:108735. doi: 10.1016/j.biopha.2019.108735. Epub 2019 Feb 27.
Sodium ferulate (SF) is the sodium salt of ferulic acid which is an active ingredient of Radix Angelica Sinensis and Ligusticum chuanxiong hort. Here, we investigated SF inhibition in a rat model of myocardial hypertrophy induced by coarctation of the abdominal aorta. Following coarctation, rats were given SF (20, 40, and 80 mg/kg/day) for 25 consecutive days. We characterized myocardial hypertrophy using myocardial hypertrophic parameters, histopathology, and gene expression of atrial natriuretic factor (ANF) -a gene related to myocardial hypertrophy. We detected the levels of angiotensin II (Ang II) and endothelin-1 (ET-1), protein kinase C beta (PKC-β), Raf-1, extracellular regulated protein kinase 1/2 (ERK1/2), and mitogen-activated protein kinase phosphatase-1 (MKP-1) in myocardium. Notably, coarctation of the abdominal aorta increases myocardial hypertrophic parameters, cardiac myocyte diameter, the concentration of Ang II and ET-1 in myocardium, and gene expression of ANF. SF significantly ameliorates myocardial hypertrophy caused by coarctation of the abdominal aorta; reduces concentrations of Ang II and ET-1; suppresses the overexpression of ANF, PKC-β, Raf-1, and ERK1/2; and increases the expression of MKP-1. These results indicate that SF alleviates myocardial hypertrophy induced by coarctation of the abdominal aorta, and these protective effects could be related to the inhibition of PKC and mitogen-activated protein kinase (MAPK) signaling pathways.
阿魏酸钠（SF）是当归和川芎中的活性成分阿魏酸的钠盐。在这里，我们研究了 SF 在腹主动脉缩窄诱导的大鼠心肌肥厚模型中的抑制作用。腹主动脉缩窄后，大鼠连续 25 天给予 SF（20、40 和 80mg/kg/天）。我们通过心肌肥厚参数、组织病理学和与心肌肥厚相关的心房利钠肽（ANF）基因的表达来表征心肌肥厚。我们检测了血管紧张素 II（Ang II）和内皮素-1（ET-1）、蛋白激酶 Cβ（PKC-β）、Raf-1、细胞外调节蛋白激酶 1/2（ERK1/2）和丝裂原活化蛋白激酶磷酸酶-1（MKP-1）在心肌中的水平。值得注意的是，腹主动脉缩窄增加了心肌肥厚参数、心肌细胞直径、心肌中 Ang II 和 ET-1 的浓度以及 ANF 的基因表达。SF 显著改善了腹主动脉缩窄引起的心肌肥厚；降低 Ang II 和 ET-1 的浓度；抑制 ANF、PKC-β、Raf-1 和 ERK1/2 的过度表达；并增加 MKP-1 的表达。这些结果表明 SF 减轻了腹主动脉缩窄引起的心肌肥厚，这些保护作用可能与抑制蛋白激酶 C 和丝裂原活化蛋白激酶（MAPK）信号通路有关。
