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Article Open Access

Luteolin suppresses lipopolysaccharide‑induced cardiomyocyte hypertrophy and autophagy in vitro

  • Authors:
    • Xing Li
    • Jian Liu
    • Jianfeng Wang
    • Donghua Zhang
  • View Affiliations / Copyright

    Affiliations: Teaching and Research Section of Traditional Chinese Medicine, Jiangsu Jiankang Vocational College, Nanjing, Jiangsu 210018, P.R. China, Department of Cardiovascular Medicine, Affiliated Hospital of Nanjing University of Traditional Chinese Medicine, Nanjing, Jiangsu 210029, P.R. China, China Pharmaceutical University, Nanjing, Jiangsu 210009, P.R. China
    Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1551-1560
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    Published online on: January 2, 2019
       https://doi.org/10.3892/mmr.2019.9803
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Abstract

Luteolin (LTL) serves essential roles in a wide variety of biological processes. Lipopolysaccharide (LPS) can lead to myocardial hypertrophy and autophagy. However, the roles of LTL on LPS‑induced cardiomyocyte hypertrophy and autophagy in rat cardiomyocytes have not yet been fully elucidated. In the present study, the morphology of cultured rat cardiomyocytes was observed under an inverted microscope. Cell viability was detected by MTT assay. α‑Actinin and microtubule‑associated protein 1 light chain 3 (LC3) expression levels were measured by immunofluorescence assay. In addition, the expression levels of atrial natriuretic peptide/brain natriuretic peptide (ANP/BNP), LC3, and autophagy‑ and Wnt signaling pathway‑associated genes were analyzed by reverse transcription‑quantitative polymerase chain reaction or western blot assays. The results indicated that LTL increased the cell viability of cardiomyocytes treated with LPS. LTL decreased the expression of cardiac hypertrophy associated markers (ANP and BNP). LTL decreased α‑actinin and LC3 expression levels in LPS‑treated cardiomyocytes. It was also demonstrated that LTL suppressed the mRNA and protein expression levels of LPS‑mediated autophagy and Wnt signaling pathway‑associated genes. In addition, it was demonstrated that silencing of β‑catenin inhibited LPS‑induced cardiomyocyte hypertrophy and the formation of autophagosomes. Thus, the present study suggested that LTL protected against LPS‑induced cardiomyocyte hypertrophy and autophagy in rat cardiomyocytes.
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Copy and paste a formatted citation
Spandidos Publications style
Li X, Liu J, Wang J and Zhang D: Luteolin suppresses lipopolysaccharide‑induced cardiomyocyte hypertrophy and autophagy in vitro. Mol Med Rep 19: 1551-1560, 2019.
APA
Li, X., Liu, J., Wang, J., & Zhang, D. (2019). Luteolin suppresses lipopolysaccharide‑induced cardiomyocyte hypertrophy and autophagy in vitro. Molecular Medicine Reports, 19, 1551-1560. https://doi.org/10.3892/mmr.2019.9803
MLA
Li, X., Liu, J., Wang, J., Zhang, D."Luteolin suppresses lipopolysaccharide‑induced cardiomyocyte hypertrophy and autophagy in vitro". Molecular Medicine Reports 19.3 (2019): 1551-1560.
Chicago
Li, X., Liu, J., Wang, J., Zhang, D."Luteolin suppresses lipopolysaccharide‑induced cardiomyocyte hypertrophy and autophagy in vitro". Molecular Medicine Reports 19, no. 3 (2019): 1551-1560. https://doi.org/10.3892/mmr.2019.9803
Copy and paste a formatted citation
x
Spandidos Publications style
Li X, Liu J, Wang J and Zhang D: Luteolin suppresses lipopolysaccharide‑induced cardiomyocyte hypertrophy and autophagy in vitro. Mol Med Rep 19: 1551-1560, 2019.
APA
Li, X., Liu, J., Wang, J., & Zhang, D. (2019). Luteolin suppresses lipopolysaccharide‑induced cardiomyocyte hypertrophy and autophagy in vitro. Molecular Medicine Reports, 19, 1551-1560. https://doi.org/10.3892/mmr.2019.9803
MLA
Li, X., Liu, J., Wang, J., Zhang, D."Luteolin suppresses lipopolysaccharide‑induced cardiomyocyte hypertrophy and autophagy in vitro". Molecular Medicine Reports 19.3 (2019): 1551-1560.
Chicago
Li, X., Liu, J., Wang, J., Zhang, D."Luteolin suppresses lipopolysaccharide‑induced cardiomyocyte hypertrophy and autophagy in vitro". Molecular Medicine Reports 19, no. 3 (2019): 1551-1560. https://doi.org/10.3892/mmr.2019.9803
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