Open Access

Luteolin attenuates sepsis‑induced myocardial injury by enhancing autophagy in mice

  • Authors:
    • Bin Wu
    • Haixu Song
    • Miaomiao Fan
    • Fei You
    • Liang Zhang
    • Jian Luo
    • Junzhi Li
    • Lingpeng Wang
    • Congye Li
    • Ming Yuan
  • View Affiliations

  • Published online on: March 11, 2020     https://doi.org/10.3892/ijmm.2020.4536
  • Pages: 1477-1487
  • Copyright: © Wu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Sepsis‑induced cardiomyopathy (SIC) is a complication of severe sepsis and septic shock characterized by an invertible myocardial depression. This study sought to explore the potential effects and mechanism of luteolin, a flavonoid polyphenolic compound, in lipopolysaccharide (LPS)‑induced myocardial injury. Experimental mice were randomly allocated into 3 groups (25 mice in each group): The control group (NC), the LPS group (LPS) and the LPS + luteolin group (LPS + Lut). Before the SIC model was induced, luteolin was dissolved in DMSO and injected intraperitoneally for 10 days into LPS + Lut group mice. NC group and LPS group mice received an equal volume of DMSO for 10 days. On day 11, the animal model of sepsis‑induced cardiac dysfunction was induced by intraperitoneal injection of LPS. A total of 12 h after LPS injection, measurements and comparisons were made among the groups. Luteolin administration improved cardiac function, attenuated the inflammatory response, alleviated mitochondrial injury, decreased oxidative stress, inhibited cardiac apoptosis and enhanced autophagy. In addition, luteolin significantly decreased the phosphorylation of AMP‑activated protein kinase (AMPK) in septic heart tissue. The protective effect of luteolin was abolished by 3‑methyladenine (an autophagy inhibitor) and dorsomorphin (compound C, an AMPK inhibitor), as evidenced by decreased autophagic activity, destabilized mitochondrial membrane potential and increased apoptosis in LPS‑treated cardiomyocytes, but was mimicked by 5‑aminoimidazole‑4‑carboxamide ribonucleotide (an AMPK activator), suggesting that luteolin attenuates LPS‑induced myocardial injury by increasing autophagy through AMPK activation. Luteolin may be a promising therapeutic agent for treating SIC.

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May 2020
Volume 45 Issue 5

Print ISSN: 1107-3756
Online ISSN:1791-244X

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APA
Wu, B., Song, H., Fan, M., You, F., Zhang, L., Luo, J. ... Yuan, M. (2020). Luteolin attenuates sepsis‑induced myocardial injury by enhancing autophagy in mice. International Journal of Molecular Medicine, 45, 1477-1487. https://doi.org/10.3892/ijmm.2020.4536
MLA
Wu, B., Song, H., Fan, M., You, F., Zhang, L., Luo, J., Li, J., Wang, L., Li, C., Yuan, M."Luteolin attenuates sepsis‑induced myocardial injury by enhancing autophagy in mice". International Journal of Molecular Medicine 45.5 (2020): 1477-1487.
Chicago
Wu, B., Song, H., Fan, M., You, F., Zhang, L., Luo, J., Li, J., Wang, L., Li, C., Yuan, M."Luteolin attenuates sepsis‑induced myocardial injury by enhancing autophagy in mice". International Journal of Molecular Medicine 45, no. 5 (2020): 1477-1487. https://doi.org/10.3892/ijmm.2020.4536