Pioglitazone Ameliorates Renal Ischemia-Reperfusion Injury via Inhibition of NF-κB Activation and Inflammation in Rats

Renal ischemia-reperfusion injury (IRI) is considered as a major cause of acute kidney injury. In this study, we investigated the role of the NF-kappa B signaling pathway and inflammation in the amelioration of renal IRI using pioglitazone. Sprague-Dawley (SD) rats were subjected to bilateral renal artery clamping for 45 min followed by perfusion restoration for establishing a simulated renal IRI model. At 24 h post-operatively, we assessed the serum levels of creatinine and urea nitrogen, expression levels of peroxisome proliferator-activated receptor gamma (PPAR-gamma) and NF-kappa B-related (p-IKK-beta and I kappa B-alpha) proteins, and mRNA expression levels of the inflammatory cytokines, including TNF-alpha and MCP-1, in the renal tissue of various study groups. The histopathological evaluation of renal tissue was also conducted. In rat renal tissue, pioglitazone treatment decreased the serum levels of post-renal IRI creatinine and urea nitrogen, as well as necrosis. Furthermore, it elevated the expression of PPAR-gamma protein and decreased the expression of NF-kappa B-related proteins. Pioglitazone also decreased the mRNA expression of TNF-alpha and MCP-1 in the renal tissue. Thus, pioglitazone ameliorates renal IRI by inhibiting the NF-kappa B signaling pathway and inflammatory response in rats.