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Abstract : In critically ill patients, acute kidney damage (AKI) is a frequent consequence that is linked to higher morbidity and mortality. The most typical cause of AKI is sepsis. Ibudilast is a strong inhibitor of phosphodiesterase (PDE)-4 and other PDE subtypes as well as a TLR-4 antagonist. To examine the nephroprotective effect of Ibudilast by their anti-inflammatory, antioxidant effect and modulation of apoptosis through their effect on TLR- 4/NF- kB signaling pathway in experimental model of sepsis. 24 adult male mice divided randomly in to 4 groups (Sham group, cecal ligation and puncture (CLP) group, Vehicle group, Ibudilast (10 mg/kg) treatment group). We sacrificed the animals after 24 hours, and each mouse's blood sample was drawn. To identify markers (tumor necrosis factor alpha (TNF-α), interleukin- 6 (IL-6), macrophage migration inhibitory factor (MIF), interleukin- 10 (IL-10), F2-isoprostane, caspae-3, B-cell lymphoma-2 (Bcl-2), toll like receptor- 4 (TLR-4) in kidney homogenate. Part of the kidney was studied for histopathology. Ibudilast significantly reduced TNF-α, IL-6, MIF, induced IL-10, lowered F2-isoprostane, dropped caspae-3, rose Bcl-2, lowered toll like receptor- 4 protein expression, reduced blood urea and reduced serum creatinine. Ibudilast lessens kidney damage induced by sepsis through blocking TLR-4/NF-kB downstream signal transduction pathways, oxidative stress and modulation of apoptosis.

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