Sodium Ferulate Protects against Angiotensin II-Induced Cardiac Hypertrophy in Mice by Regulating the MAPK/ERK and JNK Pathways

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.

Oolong tea prevents cardiomyocyte loss against hypoxia by attenuating p‐JNK mediated hypertrophy and enhancing P‐IGF1R, p‐akt, and p‐Badser136 activity and by fortifying NRF2 antioxidation system

“…Elevation in ROS generation including superoxide anions, H 2 O 2 , and hydroxyl radicals has known to activate the MAPKs to induce hypertrophic effects and elimination of these ROS by scavengers or antioxidants potentially attenuates cardiac hypertrophy . In our recent study administration of superoxide anion scavenger on rats hearts suppresses hypoxia associated cardiac apoptosis in rats with sleep apnea by elevating IGFI associated survival pathway and by enhancing the phosphorylation of Bad .…”

“…Various alternative medicines are been evaluated for their potential to establish cardiac protection . Our previous studies and several other reports show that activation of pJNK and p38 MAPKs play an important role in cardiac hypertrophic effects and associated apoptosis . Activation of ERK, JNK and p38 MAPKs stimulates the expression of early proteins of hypertrophy, like the c ‐ Fos and c ‐ Jun and promotes hypertrophy and apoptosis, therefore, the role of MAPKs is involved in the pathogenesis of cardiac hypertrophy …”

The Long Noncoding RNA 150Rik Promotes Mesangial Cell Proliferation via miR-451/IGF1R/p38 MAPK Signaling in Diabetic Nephropathy

“…IGF1R is a protein and transmembrane tyrosine protein receptor which is involved in the IGF1/MAPK signalling pathway [48,49]. P38MAPK, an important member of the MAPK signalling pathway, can activate the MAPK signalling pathway [50][51][52][53], causing the proliferation of cells [54][55][56]. Moreover, our previous studies have shown that p38MAPK signalling is inhibited by miR-451 in early DN [15].…”

Protective effects of resveratrol improve cardiovascular function in rats with diabetes

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