GSK-3β Inhibitor 17 (compound 5 n) reduces the expression of p-p65 and KIM-1 proteins in a dose-dependent manner (16, 32, 64 µM) induced by cisplatin. Additionally, at a concentration of 32 µM, it decreases the levels of TNF-α, IL-1β, IL-6, and MCP-1 mRNA in an acute kidney injury (AKI) model of HK-2 cells triggered by cisplatin.

GSK-3β Inhibitor 17 (compound 5 n) reduces the expression of p-p65 and KIM-1 proteins in a dose-dependent manner (16, 32, 64 µM) induced by cisplatin. Additionally, at a concentration of 32 µM, it decreases the levels of TNF-α, IL-1β, IL-6, and MCP-1 mRNA in an acute kidney injury (AKI) model of HK-2 cells triggered by cisplatin.

In an experimental study, the GSK-3β inhibitor 17 administered intraperitoneally (i.p.) at doses of 12.5, 25, and 50 mg/kg was shown to mitigate kidney damage by reducing the activation of the NF-κB signaling pathway and the release of inflammatory cytokines induced by cisplatin. The study used male C57/BL6 mice aged 6-8 weeks and weighing 20-22 g, treated with cisplatin (20 mg/kg i.p.) for three days. The inhibitor was administered 24 hours prior to modeling. Results indicated a significant reduction in cisplatin-induced renal glycogen accumulation and tubular necrosis. Additionally, the treatment notably decreased the protein level of phosphorylated P65 and downregulated the mRNA expression of TNF-α, IL-1β, IL-6, and MCP-1 in the cisplatin-treated groups.