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Updated: May 23, 2026
Ischemia-reperfusion Model of Acute Kidney Injury and Post Injury Fibrosis in Mice
Published on: August 9, 2013
Protective effects of pioglitazone on renal ischemia-reperfusion injury in mice
Honglin Hu1, Cong Zou, Xiaoqing Xi
1Department of Urology, Second Affiliated Hospital of Nanchang University, Nanchang, PR China. honglinhu@126.com
Background:
Renal ischemia-reperfusion injury (IRI) is a complex pathophysiologic process involving cell apoptosis and oxidant damages that leads to acute renal failure in both native kidneys and renal allografts. Pioglitazone is a novel class of oral antidiabetic agents currently used to treat type 2 diabetes mellitus. Pioglitazone exerts protective effects on acute myocardial ischemia and acute cerebral ischemia. The aim of this study was to investigate the possible beneficial effects of pioglitazone on renal IRI in mice.
Methods:
IRI was induced by bilateral renal ischemia for 45 min followed by reperfusion. Fifty-five healthy male Balb/c mice were randomly assigned to one of the following groups: PBS + IRI, pioglitazone + IRI, PBS + sham IRI, pioglitazone + sham IRI. Kidney function tests, histopathologic examination, renal cell Bcl-2, and Bax expression were determined 24 h after reperfusion. Animals' survival was examined 7 days after operation.
Results:
Animals pretreated with pioglitazone had lower plasma levels of blood urea nitrogen and creatinine caused by IRI, lower histopathologic scores, and improved survival rates following IRI. Renal cell apoptosis induced by IRI was abrogated in kidneys of mice pretreated by pioglitazone, with an increase in Bcl-2 expression and a decrease in Bax expression. Furthermore, pioglitazone pretreatment protected against lethal renal IRI.
Conclusions:
Peroxisome proliferator-activated receptor activation by pioglitazone exerts protective effects on renal IRI in mice by abrogating renal cell apoptosis. Thus, pioglitazone could be a novel therapeutic tool in renal IRI.
Insights
Pioglitazone pretreatment protects against kidney injury from ischemia-reperfusion (IRI) in mice. It reduces cell apoptosis and improves survival, suggesting pioglitazone as a potential therapeutic for renal IRI.
Area of Science:
- Nephrology
- Pharmacology
- Cell Biology
Background:
- Renal ischemia-reperfusion injury (IRI) causes acute kidney injury via apoptosis and oxidative stress.
- Pioglitazone, an antidiabetic drug, shows protective effects in myocardial and cerebral ischemia.
- This study investigates pioglitazone's efficacy in preventing renal IRI.
Purpose of the Study:
- To evaluate the renoprotective effects of pioglitazone against IRI in a mouse model.
- To assess the impact of pioglitazone on renal function, apoptosis, and survival post-IRI.
Main Methods:
- Renal IRI was induced in mice by 45 minutes of ischemia followed by reperfusion.
- Mice were pretreated with either pioglitazone or PBS.
- Kidney function, histopathology, apoptosis markers (Bcl-2, Bax), and survival were assessed.
Main Results:
- Pioglitazone pretreatment significantly reduced blood urea nitrogen and creatinine levels.
- Histopathological scores were lower, and survival rates were improved in pioglitazone-treated mice.
- Pioglitazone abrogated renal cell apoptosis by increasing Bcl-2 and decreasing Bax expression.
Conclusions:
- Pioglitazone activation of peroxisome proliferator-activated receptor protects against renal IRI in mice.
- The protective mechanism involves the abrogation of renal cell apoptosis.
- Pioglitazone shows promise as a novel therapeutic agent for renal IRI.
