Please have in mind, though, that base pay estimates can be off by as much as 20% because they average out not only junior, but also mid and senior positions. Acute liver injury (ALI) is recognized as a serious complication of sepsis in patients in intensive care units (ICUs). S100A8/A9 is known to promote inflammation and immune responses. However, the role of S100A8/A9 in the regulation of sepsis-induced ALI remains known. Our results indicated that S100A8/A9 expression was significantly upregulated in the livers of septic mice 24 h after cecal ligation and a puncture (CLP) operation. Moreover, S100A9-KO in mice markedly attenuated CLP-induced liver dysfunction and injury, promoting the AMPK/ACC/GLUT4-mediated increases in fatty acid and glucose uptake as well as the improvement in mitochondrial function and ATP production. In contrast, treatment with the AMPK inhibitor Compound C reversed the inhibitory effects of S100A9 KO on CLP-induced liver dysfunction and injury in vivo. Finally, the administration of the S100A9 inhibitor Paquinimod (Paq) to WT mice protected against CLP-induced mortality, liver injury and mitochondrial dysfunction. In summary, our findings demonstrate for the first time that S100A9 plays an important pro-inflammatory role in sepsis-mediated ALI by regulating AKT-AMPK-dependent mitochondrial energy metabolism and highlights that targeting S100A9 may be a promising new approach for the prevention and treatment of sepsis-related liver injury. Sepsis is a common complication after infection, shock and severe trauma, and it is one of the major causes of mortality in patients in intensive care units (ICUs). Upon pathogen infection, the host innate immune system is excessively activated innate immune activation is followed by and causes the occurrence of a cytokine storm, which is characterized by high levels of pro-inflammatory cytokines, including TNF-α, IL-1β, IL-6, and IFN-γ, and results in cell death and multiple organ dysfunction.
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