Document Type
Article
Publication Date
2023
Abstract
Aim: Cilostazol was investigated as a protective agent against lipopolysaccharide (LPS)-associated acute kidney damage in mice. Methods: Cilostazol (50 mg/kg/day; p.o.) administered for 7 consecutive days before a single LPS dose (2 mg/kg; i.p.). Results: Cilostazol hampered serum creatinine, cystatin C, and renal kidney injury molecule-1 and neutrophil gelatinaseassociated lipocalin; repressed toll-like receptor 4 and MyD88 transcription, as well as nuclear factor-kappa B p65, interleukin-1b, and malondialdehyde content; and boosted Nrf2 mRNA expression, hemeoxygenase-1 activity, and reduced glutathione content. This was synchronous with an upregulation of p-phosphoinositide 3-kinase and p-Akt expressions. Conclusion: Collectively, cilostazol prevented LPS renal injury, which might correspond to modulation of toll-like receptor 4/nuclear factor-kappa B, nuclear factor erythroid 2-related factor 2/hemeoxygenase-1, and phosphoinositide 3- kinase/Akt pathways
Recommended Citation
Mohamed, Ahmed F.; Sayed, Helmy M.; Zaki, Hala F.; and Safar, Marwa, "Modulation of TLR4/NF- Modulation of TLR4/NF-κB, Nrf2/HO-1 and PI3K/Akt signaling by cilostazol mitigates lipopolysaccharide-induced septic acute kidney injury" (2023). Pharmacy. 660.
https://buescholar.bue.edu.eg/pharmacy/660