Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2017:2017:3754942.
doi: 10.1155/2017/3754942. Epub 2017 Jan 10.

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

Bo Hu  1 , Jian-Tao Song  1 , Xian-Fei Ji  1 , Zun-Qi Liu  1 , Mu-Lin Cong  1 , Dong-Xing Liu  1
Affiliations

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

Bo Hu et al. Biomed Res Int. 2017.

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.

PubMed Disclaimer

Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1
The myocardial tissue sections of different groups (HE stain, ×400). (a) HE staining showed the morphologies of different groups. ((a)-(A)) Control group; ((a)-(B)) PBS group; ((a)-(C)) AngII group; ((a)-(D)) AngII + 10 mg/kg group; ((a)-(E)) AngII + 40 mg/kg SF group; ((a)-(F)) AngII + 40 mg/kg SF + 10 mg/kg TBHQ group. (b) The cell area of different groups. Scale bar = 50 μm, ∗∗∗P < 0.01 versus control, △P < 0.05 versus Ang II, and n = 3.
Figure 2
Figure 2
The apoptosis analysis of different groups. (a) The apoptosis rate analysis and (b) the comparison of mRNA expression. ((c) and (d)) Western Blot showed the expression level of apoptosis related proteins. ∗∗∗P < 0.01 versus control, △P < 0.05 versus Ang II, and n = 3.
Figure 3
Figure 3
The mRNA expressions of ANP, TGF-β, and Col III in each group. (a) Q-PCR detected the expression of mRNA; ((b) and (c)) Western Blot showed the expression level of proteins. ∗∗∗P < 0.01 versus control, △P < 0.05 versus Ang II, and n = 3.
Figure 4
Figure 4
The expressions of ERK, p-ERK, p38MAPK, p-p38MAPK, JNK, and p-JNK in each group. ∗∗∗P < 0.01 versus control, △P < 0.05 versus Ang II, and n = 3.
See this image and copyright information in PMC

References

    1. Zhang Y., Cao Y., Duan H., Wang H., He L. Imperatorin prevents cardiac hypertrophy and the transition to heart failure via NO-dependent mechanisms in mice. Fitoterapia. 2012;83(1):60–66. doi: 10.1016/j.fitote.2011.09.011. - DOI - PubMed
    1. Grossman W., Paulus W. J. Myocardial stress and hypertrophy: a complex interface between biophysics and cardiac remodeling. Journal of Clinical Investigation. 2013;123(9):3701–3703. doi: 10.1172/jci69830. - DOI - PMC - PubMed
    1. Wu J. B., Zhou Y., Liang C. L., et al. Cyclovirobuxinum D alleviates cardiac hypertrophy in hyperthyroid rats by preventing apoptosis of cardiac cells and inhibiting the p38 mitogen-activated protein kinase signaling pathway. Chinese Journal of Integrative Medicine. 2016 doi: 10.1007/s11655-015-2299-7. - DOI - PubMed
    1. Yamakawa H., Imamura T., Matsuo T., et al. Diastolic wall stress and ANG II in cardiac hypertrophy and gene expression induced by volume overload. American Journal of Physiology—Heart and Circulatory Physiology. 2000;279(6):H2939–H2946. - PubMed
    1. Purcell N. H., Wilkins B. J., York A., et al. Genetic inhibition of cardiac ERK1/2 promotes stress-induced apoptosis and heart failure but has no effect on hypertrophy in vivo. Proceedings of the National Academy of Sciences of the United States of America. 2007;104(35):14074–14079. doi: 10.1073/pnas.0610906104. - DOI - PMC - PubMed

MeSH terms

LinkOut - more resources