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Article

Apelin protects against sepsis‑induced cardiomyopathy by inhibiting the TLR4 and NLRP3 signaling pathways

  • Authors:
    • Qiancheng Luo
    • Guorong Liu
    • Guo Chen
    • Dongfeng Guo
    • Lei Xu
    • Min Hang
    • Mingming Jin
  • View Affiliations / Copyright

    Affiliations: Department of Emergency Medicine, Shanghai Pudong New Area Gongli Hospital, The Second Military Medical University, Shanghai 200135, P.R. China, Department of Clinical Laboratory, Shanghai Gongli Hospital, The Second Military Medical University, Shanghai 200135, P.R. China
  • Pages: 1161-1167
    |
    Published online on: May 9, 2018
       https://doi.org/10.3892/ijmm.2018.3665
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Abstract

The mechanism underlying sepsis‑induced cardiomyopathy (SICM) remains unclear. The aim of the present study was therefore to illuminate the mechanisms and effects of apelin on SICM, using both patient clinical features and a sepsis rat model. A total of 73 adult patients with or without sepsis were analyzed. Male rats were used to generate the sepsis model through cecal ligation and puncture (CLP). The clinical analysis results demonstrated that sepsis induced cardiac dysfunction, including a decrease of left ventricular end‑diastolic dimension, fractional shortening, ejection fraction, left ventricular end‑systolic dimension, and stroke volume, compared with healthy controls. In addition, the results demonstrated that white blood cell count and inflammatory cytokine expression increased in sepsis patients compared with healthy controls. ELISA analyses revealed that apelin was upregulated following sepsis. The animal model study demonstrated that rats treated with apelin had significantly reduced mortality and suppressed sepsis‑induced myocardial damage and inflammatory responses, through suppression of activation of the Toll‑like receptor 4 (TLR4) and NLR family pyrin domain containing 3 (NLRP3) signaling pathways. Taken together, the present results suggested that apelin had a protective effect against sepsis‑induced cardiac impairment by attenuating TLR4 and NLRP3 signaling‑mediated inflammatory responses.
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Copy and paste a formatted citation
Spandidos Publications style
Luo Q, Liu G, Chen G, Guo D, Xu L, Hang M and Jin M: Apelin protects against sepsis‑induced cardiomyopathy by inhibiting the TLR4 and NLRP3 signaling pathways. Int J Mol Med 42: 1161-1167, 2018.
APA
Luo, Q., Liu, G., Chen, G., Guo, D., Xu, L., Hang, M., & Jin, M. (2018). Apelin protects against sepsis‑induced cardiomyopathy by inhibiting the TLR4 and NLRP3 signaling pathways. International Journal of Molecular Medicine, 42, 1161-1167. https://doi.org/10.3892/ijmm.2018.3665
MLA
Luo, Q., Liu, G., Chen, G., Guo, D., Xu, L., Hang, M., Jin, M."Apelin protects against sepsis‑induced cardiomyopathy by inhibiting the TLR4 and NLRP3 signaling pathways". International Journal of Molecular Medicine 42.2 (2018): 1161-1167.
Chicago
Luo, Q., Liu, G., Chen, G., Guo, D., Xu, L., Hang, M., Jin, M."Apelin protects against sepsis‑induced cardiomyopathy by inhibiting the TLR4 and NLRP3 signaling pathways". International Journal of Molecular Medicine 42, no. 2 (2018): 1161-1167. https://doi.org/10.3892/ijmm.2018.3665
Copy and paste a formatted citation
x
Spandidos Publications style
Luo Q, Liu G, Chen G, Guo D, Xu L, Hang M and Jin M: Apelin protects against sepsis‑induced cardiomyopathy by inhibiting the TLR4 and NLRP3 signaling pathways. Int J Mol Med 42: 1161-1167, 2018.
APA
Luo, Q., Liu, G., Chen, G., Guo, D., Xu, L., Hang, M., & Jin, M. (2018). Apelin protects against sepsis‑induced cardiomyopathy by inhibiting the TLR4 and NLRP3 signaling pathways. International Journal of Molecular Medicine, 42, 1161-1167. https://doi.org/10.3892/ijmm.2018.3665
MLA
Luo, Q., Liu, G., Chen, G., Guo, D., Xu, L., Hang, M., Jin, M."Apelin protects against sepsis‑induced cardiomyopathy by inhibiting the TLR4 and NLRP3 signaling pathways". International Journal of Molecular Medicine 42.2 (2018): 1161-1167.
Chicago
Luo, Q., Liu, G., Chen, G., Guo, D., Xu, L., Hang, M., Jin, M."Apelin protects against sepsis‑induced cardiomyopathy by inhibiting the TLR4 and NLRP3 signaling pathways". International Journal of Molecular Medicine 42, no. 2 (2018): 1161-1167. https://doi.org/10.3892/ijmm.2018.3665
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