Abstract
Background and Objective. It has been reported that sodium ferulate (SF) has hematopoietic function against anemia and immune regulation, inflammatory reaction inhibition, inhibition of tumor cell proliferation, cardiovascular and cerebrovascular protection, and other functions. Thus, this study aimed to investigate the effects of SF on angiotensin II- (AngII-) induced cardiac hypertrophy in mice through the MAPK/ERK and JNK signaling pathways. Methods. Seventy-two male C57BL/6J mice were selected and divided into 6 groups: control group, PBS group, model group (AngII), model + low-dose SF group (AngII + 10 mg/kg SF), model + high-dose SF group (AngII + 40 mg/kg SF), and model + high-dose SF + agonist group (AngII + 40 mg/kg SCU + 10 mg/kg TBHQ). After 7 d/14 d/28 days of treatments, the changes of blood pressure and heart rates of mice were compared. The morphology of myocardial tissue and the apoptosis rate of myocardial cells were observed. The mRNA and protein expressions of atrial natriuretic peptide (ANP), transforming growth factor-β (TGF-β), collagen III (Col III), and MAPK/ERK and JNK pathway-related proteins were detected after 28 days of treatments. Results. SF improved the mice's cardiac abnormality and decreased the apoptosis rate of myocardial cells in a time- and dose-dependent manner (all P < 0.05). MAPK/ERK pathway activator inhibited the protective effect of SF in myocardial tissue of mice (P < 0.05). SF could inhibit the expression of p-ERK, p-p38MAPK, and p-JNK and regulate the expressions of ANP, TGF-β, and Col III (all P < 0.05). Conclusion. Our findings provide evidence that SF could protect against AngII-induced cardiac hypertrophy in mice by downregulating the MAPK/ERK and JNK pathways.
Highlights
Cardiac hypertrophy is the common lesion of various cardiovascular diseases, including hypertension, myocardial infarction, and congenital heart disease and the leading cause of the occurrence of heart failure and sudden death to the patients with the above diseases [1]
Studies on the levels of whole body and organs as well as experiments on cultured cells have successively confirmed that Angiotensin II (AngII) has a direct effect on promoting cardiac hypertrophy [10, 11]
This study used the method of continuous-pumping-AngII into the backs of male C57BL/6 mice to establish the model of cardiac hypertrophy and the control group without placing-in micropumps
Summary
Cardiac hypertrophy is the common lesion of various cardiovascular diseases, including hypertension, myocardial infarction, and congenital heart disease and the leading cause of the occurrence of heart failure and sudden death to the patients with the above diseases [1]. It is found that the expression level of phosphorylated ERK (p-ERK) commonly existing in the myocardial tissues of patients with pathologic cardiac hypertrophy is increased but its mechanism has not been clearly studied [5, 6]. This study aimed to investigate the effects of SF on angiotensin II- (AngII-) induced cardiac hypertrophy in mice through the MAPK/ERK and JNK signaling pathways. The mRNA and protein expressions of atrial natriuretic peptide (ANP), transforming growth factor-β (TGF-β), collagen III (Col III), and MAPK/ERK and JNK pathway-related proteins were detected after 28 days of treatments. MAPK/ERK pathway activator inhibited the protective effect of SF in myocardial tissue of mice (P < 0.05). Our findings provide evidence that SF could protect against AngII-induced cardiac hypertrophy in mice by downregulating the MAPK/ERK and JNK pathways
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