biostudies-literatureUnknown61(4)Kim DK<h4>Purpose</h4>Despite the role of carbon monoxide in ameliorating ischemia-reperfusion injury (IRI), its use in the clinical setting is restricted owing to its toxicity. Herein, we investigated the <i>in vivo</i> effects of carbon monoxide-releasing molecule-3 (CORM-3) on IRI.<h4>Materials and methods</h4>Fifteen rats were equally and randomly divided into three groups: sham (right nephrectomy), control (right nephrectomy and left renal ischemia), and CORM-3 (right nephrectomy and CORM-3 injection before left renal ischemia). Kidney tissues and blood samples collected from sacrificed rats were evaluated to determine the renoprotective effect and mechanism of CORM-3.<h4>Results</h4>Concentrations of serum creatinine and kidney injury molecule-1 in the CORM-3 group were significantly lower than in the control group after 75 minutes of IRI (1.2 vs. 2.4 mg/dL, p=0.01, and 292 vs. 550 pg/mL, p<0.001, respectively). Furthermore, the CORM-3 group exhibited a higher portion of normal tubules and glomeruli. TUNEL staining revealed fewer apoptotic renal tubular cells in the CORM-3 group than in the control group. The expression of 960 genes in the CORM-3 group was also altered. Pretreatment with CORM-3 before renal IRI produced a significant renoprotective effect. Fifteen of the altered genes were found to be involved in the peroxisome proliferator-activated receptors signaling pathway, and the difference in the expression of these genes between the CORM-3 and control groups was statistically significant (p<0.001).<h4>Conclusions</h4>CORM-3 ameliorates IRI by decreasing apoptosis and may be a novel strategy for protection against renal warm IRI.Investigative and clinical urology441-451https://www.ebi.ac.uk/biostudies/studies/S-EPMC7329640biostudies-literatureCarbon monoxide-releasing molecule-3: Amelioration of renal ischemia reperfusion injury in a rat model.PMC7329640Moon HSYoon YEChoi HYLee JKim YTShin SJPark SYKim DKfalseCarbon monoxide-releasing molecule-3: Amelioration of renal ischemia reperfusion injury in a rat model.<h4>Purpose</h4>Despite the role of carbon monoxide in ameliorating ischemia-reperfusion injury (IRI), its use in the clinical setting is restricted owing to its toxicity. Herein, we investigated the <i>in vivo</i> effects of carbon monoxide-releasing molecule-3 (CORM-3) on IRI.<h4>Materials and methods</h4>Fifteen rats were equally and randomly divided into three groups: sham (right nephrectomy), control (right nephrectomy and left renal ischemia), and CORM-3 (right nephrectomy and CORM-3 injection before left renal ischemia). Kidney tissues and blood samples collected from sacrificed rats were evaluated to determine the renoprotective effect and mechanism of CORM-3.<h4>Results</h4>Concentrations of serum creatinine and kidney injury molecule-1 in the CORM-3 group were significantly lower than in the control group after 75 minutes of IRI (1.2 vs. 2.4 mg/dL, p=0.01, and 292 vs. 550 pg/mL, p<0.001, respectively). Furthermore, the CORM-3 group exhibited a higher portion of normal tubules and glomeruli. TUNEL staining revealed fewer apoptotic renal tubular cells in the CORM-3 group than in the control group. The expression of 960 genes in the CORM-3 group was also altered. Pretreatment with CORM-3 before renal IRI produced a significant renoprotective effect. Fifteen of the altered genes were found to be involved in the peroxisome proliferator-activated receptors signaling pathway, and the difference in the expression of these genes between the CORM-3 and control groups was statistically significant (p<0.001).<h4>Conclusions</h4>CORM-3 ameliorates IRI by decreasing apoptosis and may be a novel strategy for protection against renal warm IRI.2020-01-01T00:00:00Z2020 Jul2025-04-04T13:25:48.278Z2025-04-04T13:25:48.278ZS-EPMC73296403266600210.4111/icu.2020.61.4.441