Abstract
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-κB 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-γ) and NF-κB-related (p-IKK-β and IκB-α) proteins, and mRNA expression levels of the inflammatory cytokines, including TNF-α 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-γ protein and decreased the expression of NF-κB-related proteins. Pioglitazone also decreased the mRNA expression of TNF-α and MCP-1 in the renal tissue. Thus, pioglitazone ameliorates renal IRI by inhibiting the NF-κB signaling pathway and inflammatory response in rats.
Highlights
Renal ischemia-reperfusion injury (IRI) is a common pathophysiological phenomenon in clinical settings
The blood glucose level increased significantly at 1 h after feeding compared to that before feeding in both groups, there were no significant differences in the blood glucose levels before and 1 h after feeding, respectively, between the control and pioglitazone treatment group
The increase in the serum creatinine and urea nitrogen levels was significantly suppressed in renal IRI rats that were treated with pioglitazone
Summary
Renal ischemia-reperfusion injury (IRI) is a common pathophysiological phenomenon in clinical settings. It is considered as a major cause of acute renal failure and the main factor in early recovery of renal graft function and long-term survival post renal transplantation. It is believed that an increase in free radical production, intracellular calcium overload, and excessive activation of inflammatory response are cumulatively responsible for IRI. The microvascular and parenchymal organ damage induced upon ischemia tissue reperfusion is mainly attributed to the reactive oxygen-free radicals, and it has been demonstrated in many organs. The production of antioxidant enzymes that scavenge free radicals in ischemic tissue is impaired, thereby exacerbating the damage caused by these free radicals in the post ischemic reperfusion tissue
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