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Molecular Medicine Reports
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October-2017 Volume 16 Issue 4

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Article Open Access

Sanggenon C protects against pressure overload‑induced cardiac hypertrophy via the calcineurin/NFAT2 pathway

  • Authors:
    • Lili Xiao
    • Yulei Gu
    • Lu Gao
    • Jiahong Shangguan
    • Yang Chen
    • Yanzhou Zhang
    • Ling Li

  • View Affiliations / Copyright

    Affiliations: Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China
    Copyright: © Xiao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 5338-5346
    |
    Published online on: August 18, 2017
       https://doi.org/10.3892/mmr.2017.7288
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Abstract

The effects of Sanggenon C on oxidative stress and inflammation have previously been reported; however, little is currently known regarding the effects of Sanggenon C on cardiac hypertrophy and fibrosis. In the present study, aortic banding (AB) was performed on mice to induce cardiac hypertrophy. After 1 week AB surgery, mice were treated daily with 10 or 20 mg/kg Sanggenon C for 3 weeks. Subsequently, cardiac function was detected using echocardiography and catheter‑based measurements of hemodynamic parameters. In addition, the extent of cardiac hypertrophy was evaluated by pathological staining and molecular analysis of heart tissue in each group. After 4 weeks of AB, vehicle‑treated mice exhibited cardiac hypertrophy, fibrosis, and deteriorated systolic and diastolic function, whereas treatment with 10 and 20 mg/kg Sanggenon C treatment ameliorated these alterations, as evidenced by attenuated cardiac hypertrophy and fibrosis, and preserved cardiac function. Furthermore, AB‑induced activation of calcineurin and nuclear factor of activated T cells 2 (NFAT2) was reduced following Sanggenon C treatment. These results suggest that Sanggenon C may exert protective effects against cardiac hypertrophy and fibrosis via suppression of the calcineurin/NFAT2 pathway.

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Copy and paste a formatted citation
Spandidos Publications style
Xiao L, Gu Y, Gao L, Shangguan J, Chen Y, Zhang Y and Li L: Sanggenon C protects against pressure overload‑induced cardiac hypertrophy via the calcineurin/NFAT2 pathway. Mol Med Rep 16: 5338-5346, 2017.
APA
Xiao, L., Gu, Y., Gao, L., Shangguan, J., Chen, Y., Zhang, Y., & Li, L. (2017). Sanggenon C protects against pressure overload‑induced cardiac hypertrophy via the calcineurin/NFAT2 pathway. Molecular Medicine Reports, 16, 5338-5346. https://doi.org/10.3892/mmr.2017.7288
MLA
Xiao, L., Gu, Y., Gao, L., Shangguan, J., Chen, Y., Zhang, Y., Li, L."Sanggenon C protects against pressure overload‑induced cardiac hypertrophy via the calcineurin/NFAT2 pathway". Molecular Medicine Reports 16.4 (2017): 5338-5346.
Chicago
Xiao, L., Gu, Y., Gao, L., Shangguan, J., Chen, Y., Zhang, Y., Li, L."Sanggenon C protects against pressure overload‑induced cardiac hypertrophy via the calcineurin/NFAT2 pathway". Molecular Medicine Reports 16, no. 4 (2017): 5338-5346. https://doi.org/10.3892/mmr.2017.7288
Copy and paste a formatted citation
x
Spandidos Publications style
Xiao L, Gu Y, Gao L, Shangguan J, Chen Y, Zhang Y and Li L: Sanggenon C protects against pressure overload‑induced cardiac hypertrophy via the calcineurin/NFAT2 pathway. Mol Med Rep 16: 5338-5346, 2017.
APA
Xiao, L., Gu, Y., Gao, L., Shangguan, J., Chen, Y., Zhang, Y., & Li, L. (2017). Sanggenon C protects against pressure overload‑induced cardiac hypertrophy via the calcineurin/NFAT2 pathway. Molecular Medicine Reports, 16, 5338-5346. https://doi.org/10.3892/mmr.2017.7288
MLA
Xiao, L., Gu, Y., Gao, L., Shangguan, J., Chen, Y., Zhang, Y., Li, L."Sanggenon C protects against pressure overload‑induced cardiac hypertrophy via the calcineurin/NFAT2 pathway". Molecular Medicine Reports 16.4 (2017): 5338-5346.
Chicago
Xiao, L., Gu, Y., Gao, L., Shangguan, J., Chen, Y., Zhang, Y., Li, L."Sanggenon C protects against pressure overload‑induced cardiac hypertrophy via the calcineurin/NFAT2 pathway". Molecular Medicine Reports 16, no. 4 (2017): 5338-5346. https://doi.org/10.3892/mmr.2017.7288
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