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Mechanistically, quercetin treatment suppresses TLR4-dependent NF-B activation, leading to a marked reduction in pro-inflammatory cytokine production and downregulation of endothelial adhesion molecules, including intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), thereby limiting neutrophil infiltration and inflammatory cell recruitment in injured kidneys (Alhusaini et al

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