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

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.

PSTPIP2 is associated with disease severity in patients with pressure ulcer sepsis and has anti-inflammatory effects

“…Upon activation of NF-κB, degradation of IκB phosphorylation leads to phosphorylation of NF-κB p65 subunit and translocation from the cytoplasm to the nucleus to increase transcription of various inflammation-related genes, including TNF-α, IL-6, and other factors. 21,22 In order to further understand the antiinflammatory mechanism of PSTPIP2, we examined how it affected the NF-κB pathway. The results revealed that…”