1. Academic Validation
  2. Carvacrol protects mice against LPS-induced sepsis and attenuates inflammatory response in macrophages by modulating the ERK1/2 pathway

Carvacrol protects mice against LPS-induced sepsis and attenuates inflammatory response in macrophages by modulating the ERK1/2 pathway

  • Sci Rep. 2023 Aug 7;13(1):12809. doi: 10.1038/s41598-023-39665-7.
Chenghua Yan # 1 Wendong Kuang # 2 3 Liang Jin # 2 Rongliang Wang 4 Ling Niu 4 Chuanqi Xie 5 Jian Ding 6 Yongcui Liao 4 Liyuan Wang 4 Hongjiao Wan 4 Guangqiang Ma 7
Affiliations

Affiliations

  • 1 College of Traditional Chinese Medicine/College of Life Sciences, Jiangxi University of Chinese Medicine, Nanchang, 330004, China. [email protected].
  • 2 Institute of Microbiology, Jiangxi Academy of Sciences, Nanchang, 330029, China.
  • 3 State Key Laboratory of Virology, Wuhan, 430071, China.
  • 4 College of Traditional Chinese Medicine/College of Life Sciences, Jiangxi University of Chinese Medicine, Nanchang, 330004, China.
  • 5 Institute of Applied Chemistry, Jiangxi Academy of Sciences, Nanchang, 330029, China.
  • 6 The First Affiliated Hospital of Nanchang University, Nanchang, 330006, China.
  • 7 College of Traditional Chinese Medicine/College of Life Sciences, Jiangxi University of Chinese Medicine, Nanchang, 330004, China. [email protected].
  • # Contributed equally.
Abstract

Macrophages play an important role in the development of life-threatening sepsis, which is characterized by multiorgan dysfunction, through their ability to produce inflammatory cytokines. Carvacrol is a phenolic compound that has been confirmed to possess strong anti‑inflammatory activity. In this study, we mainly investigated the effect of carvacrol on lipopolysaccharide (LPS)-induced macrophage proinflammatory responses and endotoxic shock. The results showed that carvacrol significantly reduced mouse body weight loss and ameliorated pathological damage to the liver, lung, and heart under LPS-induced sepsis. Carvacrol attenuated inflammatory responses by inhibiting the LPS-induced production of inflammatory cytokine interleukin-6 (IL-6) in vivo and in vitro. Mechanistically, carvacrol inhibited IL-6 production mainly through the ERK1/2 signalling pathway in macrophages. Furthermore, carvacrol improved the survival of septic mice. This study sheds LIGHT on the role of carvacrol in the pathogenesis of LPS-induced sepsis, and thus, its potential in treating sepsis patients may be considered.

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