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Erastin Inhibits Septic Shock and Inflammatory Gene Expression via Suppression of the NF-κB Pathway. | LitMetric

AI Article Synopsis

  • Sepsis is a severe condition caused by an abnormal immune reaction to infection that can lead to serious outcomes like organ failure or death.
  • Erastin, a small molecule known to induce cell death in cancer, has been found to improve outcomes in sepsis models in mice by reducing key inflammatory markers.
  • The study indicates that erastin works by inhibiting the NF-κB signaling pathway, leading to a decreased inflammatory response and offering potential as a treatment for sepsis.

Article Abstract

Sepsis is a life-threatening condition that is caused by an abnormal immune response to infection and can lead to tissue damage, organ failure, and death. Erastin is a small molecule capable of initiating ferroptotic cell death in cancer cells. However, the function of erastin in the inflammatory response during sepsis remains unknown. Here, we showed that erastin ameliorates septic shock induced by cecal ligation and puncture or lipopolysaccharides (LPS) in mice, which was associated with a reduced production of inflammatory mediators such as nitric oxide, tumor necrosis factor (TNF)-α, and interleukin (IL)-1β. Pretreatment with erastin in bone marrow-derived macrophages (BMDMs) significantly attenuated the expression of inducible nitric oxide synthase, cyclooxygenase-2, TNF-α, and IL-1β mRNA in response to LPS treatment. Furthermore, we also showed that erastin suppresses phosphorylation of IκB kinase β, phosphorylation and degradation of IκBα, and nuclear translocation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) in LPS-stimulated BMDMs. Our findings suggest that erastin attenuates the inflammatory response by suppressing the NF-κB signaling pathway, resulting in inhibition of sepsis development. This study provides new insights regarding the potential therapeutic properties of erastin in sepsis.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6947339PMC
http://dx.doi.org/10.3390/jcm8122210DOI Listing

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