PIM1 inhibitor SMI-4a attenuated lipopolysaccharide-induced acute lung injury through suppressing macrophage inflammatory responses via modulating p65 phosphorylation.
MouseEndotoxin/LPSC57BL/6MaleIntratracheal3 h before lipopolysaccharide administration
Model: Lipopolysaccharide-induced acute lung injury
SMI-4a improved survival after lethal lipopolysaccharide, reduced lung oedema, histological injury and bronchoalveolar inflammatory cell counts, and suppressed cytokine production alongside reduced nuclear p65 and Ser276 phosphorylation.
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