Dexamethasone and TAK-242 reduce inflammation in the LPS-induced acute kidney injury (AKI) mouse model

Acute Kidney Injury (AKI) poses significant clinical challenges due to its rapid onset and high mortality rates, often exacerbated by inflammatory cytokine release and subsequent tissue damage. Elevated levels of TNF-α, IL-1β, and IL-6 in AKI patients underscore the role of inflammation in disease progression. Lipopolysaccharide (LPS) serves as a potent inducer of inflammation, reflecting its relevance in AKI pathogenesis.

In this poster we evaluate the therapeutic potential of Dexamethasone (DEX) and TAK-242 (TAK) in mitigating LPS-induced AKI using a male C57BL6 mouse model. Our experimental framework encompasses the establishment of an LPS-induced inflammatory AKI model, allowing for the assessment of key inflammatory markers and renal function in response to treatment with anti-inflammatory agents. The presented study underscores the utility of LPS-induced AKI models in drug development, providing a robust platform to investigate therapeutic interventions targeting excessive inflammation. Insights gained from this research may guide the identification of novel therapeutic targets aimed at improving outcomes in AKI and related inflammatory conditions.