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Original Research

Open Access

Icariside II regulates TLR4/NF-κB signaling pathway to improve septic lung injury

  • Yan Li1
  • Baishun Lin1,2

1Department of Respiratory Medicine, Wuhan Hankou Hospital, 430012 Wuhan, Hubei, China

2Department of Emergency, the First Affiliated Hospital of Nanhua University, 421001 Hengyang, Hunan, China

DOI: 10.22514/sv.2021.216

Submitted: 30 June 2021 Accepted: 25 August 2021

Online publish date: 11 October 2021

*Corresponding Author(s): Baishun Lin E-mail: linbaishun0119@163.com

Abstract

Sepsis is caused by the inadequate response to infection and may eventually lead to fatal organ dysfunction and a high mortality rate. Acute lung injury (ALI) caused by sepsis is an important cause of its high mortality, so effective treatment drugs are urgently needed. Icariside II (ICA II) is derived from Epimedii, a ubiquitous biological flavonoid compound. ICA II has shown multiple biological activities. ICA II alleviates LPS-induced neuroinflammation by inhibiting the TLR4 / MyD88 /NF-κB pathway, however, the possible role of icaridinin II in sepsis induced acute lung injury remains unclear. Herein, we developed a sepsis-related ALI mice model induced by LPS treatment, and found Icariside II ameliorated sepsis-related acute lung injury of mice induced by LPS. Our data further confirmed that Icariside II inhibited the inflammatory response in sepsis-related ALI mice, and ameliorated oxidative stress injury. We further revealed Icariside II inhibited the apoptosis of lung cells via TLR4-NF-κB axis. Our data therefore provided a promising therapeutic drug for the treatment of sepsis-induced ALI.


Keywords

Sepsis; Acute lung injury (ALI); Icariside II (ICA II); Apoptosis; Inflammatory response; TLR4-NF-κB


Cite and Share

Yan Li,Baishun Lin. Icariside II regulates TLR4/NF-κB signaling pathway to improve septic lung injury. Signa Vitae. 2021.doi:10.22514/sv.2021.216.

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