Fisetin Attenuates Lipopolysaccharide-Induced Acute Lung Injury by Targeting Myeloid Differentiation Factor 88.

ABSTRACT: Acute lung injury (ALI), a severe respiratory syndrome driven by dysregulated inflammatory cascades, urgently requires novel therapeutic strategies. The activation of the MyD88 (Myeloid differentiation factor 88)-mediated TLR (Toll-like receptor) inflammatory signaling pathway plays a crucial role in the pathophysiology of ALI, while minimally involving interferon-mediated responses. Targeting MyD88 offers a promising approach for ALI drug development. Here, we employed surface plasmon resonance (SPR) and in vitro anti-inflammatory screening methods to evaluate the interaction of candidate drugs with MyD88 and their anti-inflammatory activity. This was followed by anti-inflammatory verification in lipopolysaccharide (LPS)-induced ALI mice. Our findings reveal that Fisetin, a flavonoid deri

SUBMITTER: Jin Z 

PROVIDER: S-EPMC12862030 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature