Open Access

Schisandrin B attenuates pressure overload‑induced cardiac remodeling in mice by inhibiting the MAPK signaling pathway

  • Authors:
    • Fen Ai
    • Qing‑Hao Guo
    • Bo Yu
    • Wei Li
    • Xin Guo
    • Zhen Chen
  • View Affiliations

  • Published online on: October 31, 2019     https://doi.org/10.3892/etm.2019.8154
  • Pages: 4645-4652
  • Copyright: © Ai et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The aim of the current study was to investigate the effect and mechanism of schisandrin B (Sch B) on myocardial hypertrophy induced by pressure overload in mice. Male C57BL/6J mice were randomly divided into three groups: i) Sham (n=12); ii) transverse aortic constriction (TAC) (n=12); and iii) Sch B‑treated (n=12; 80 mg·kg‑1·d‑1 per gavage). The model of myocardial hypertrophy was established by constricting the descending branch of the aortic arch. Following a 4‑week treatment period, cardiac remodeling was evaluated using echocardiography and pathological and molecular analysis. Sch B improved cardiac function in the Sch B‑treated group compared with the TAC group. Moreover, the Sch B‑treated group had a smaller myocardial cell cross‑sectional area and less fibrosis compared with the TAC group. The protein expression levels of cardiac hypertrophy and fibrosis markers in the TAC group were significantly higher compared with those in the sham group. The same markers in the Sch B‑treated group were significantly lower compared with those in the TAC group. Additionally, the phosphorylation levels of the mitogen‑activated protein kinase (MAPK) signaling pathway‑associated proteins extracellular signal‑regulated kinase 1/2, c‑Jun N‑terminal kinase 1/2 and P38 mitogen‑activated protein kinase were significantly lower in the Sch B‑treated group compared with the TAC group. Further in vitro investigation demonstrated that Sch B prevented the adverse effects of angiotensin II‑induced hypertrophy and fibrosis by inhibiting the MAPK signaling pathway in H9c2 cells. In conclusion, Sch B may improve pathological myocardial remodeling and cardiac function induced by pressure overload, and its underlying mechanism may be associated with inhibition of the MAPK signaling pathway.

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December 2019
Volume 18 Issue 6

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Copy and paste a formatted citation
APA
Ai, F., Guo, Q., Yu, B., Li, W., Guo, X., & Chen, Z. (2019). Schisandrin B attenuates pressure overload‑induced cardiac remodeling in mice by inhibiting the MAPK signaling pathway. Experimental and Therapeutic Medicine, 18, 4645-4652. https://doi.org/10.3892/etm.2019.8154
MLA
Ai, F., Guo, Q., Yu, B., Li, W., Guo, X., Chen, Z."Schisandrin B attenuates pressure overload‑induced cardiac remodeling in mice by inhibiting the MAPK signaling pathway". Experimental and Therapeutic Medicine 18.6 (2019): 4645-4652.
Chicago
Ai, F., Guo, Q., Yu, B., Li, W., Guo, X., Chen, Z."Schisandrin B attenuates pressure overload‑induced cardiac remodeling in mice by inhibiting the MAPK signaling pathway". Experimental and Therapeutic Medicine 18, no. 6 (2019): 4645-4652. https://doi.org/10.3892/etm.2019.8154