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Objective To investigate the carbon monoxide releasing molecule CORM-2 mitigate the effect and mechanism of mouse renal ischemia-reperfusion injury. Baby temperature about 8-10 weeks male BALB / C mice for the study, the establishment of in situ ischemia-reperfusion injury model of mouse kidney, left renal pedicle with a vascular clamp closed, placed in a temperature of 31.5 degrees Celsius oven for 60 minutes. Vascular clips and then immediately release the left kidney to restore blood flow after resection of the right kidney. The mice were randomly divided into three groups: (1) control group, 1 hour before surgery intravenously injected into DMSO (1ml/kg); (2) experimental groups: One hour before surgery tail intravenous injection of a solution of the CORM-2 DMSO ( 10mg/kg); (3) the sham group, one hour before surgery tail vein injection into DMSO (1mL/Kg); 24 hours after detection of creatinine (Cr) and blood urea nitrogen (BUN) value, and to take control group, experimental group, sham group kidney specimens HE and PAS pathological examination of HO-1 Immunohistochemical detection of renal tissue, MPO, TUNEL expression. Mouse kidney ischemia time was extended to 80 minutes to observe the impact of CORM-2 on mice survival. Results:; control group, serum creatinine and urea nitrogen (102.21 ± 42.15) μmol / L and (56.69 ± 15.46) mmol / L,; experimental group (24.19 ± 9.99) μmol / L and (9.29 ± 4.74) mmol / L ; sham group (18.85 ± 10.24) μmol / L and (8.34 ± 4.00) mmol / L, respectively. Renal function (Cr and BUN) of the experimental group was significantly improved relative to the control group (P lt; 0.05). PAS staining revealed necrosis of tubular epithelial cells in large areas of the control group, the nucleus disappear, capillary congestion, tube formation; experimental group, there is a small amount of renal tubular epithelial cell necrosis, but the number was significantly reduced compared with the control group. The HE of diffuse large control group tubular necrosis, renal tubular epithelial cell necrosis of the experimental group was significantly reduced, most tubular near normal. Immunohistochemistry showed that very few HO-1 expression in the kidney tissue of sham group, the positive diffuse expression in the kidney tissue of the experimental group, the control group, HO-1 expression in tubular epithelial cells. Immunohistochemistry showed that the control group renal tissue MPO is abundantly expressed in the cortex and medulla, while the experimental group was significantly reduced MPO expression. The TUNEL display the control group, a large number of tubular epithelial cell necrosis disintegration, apoptotic bodies in the cytoplasm corticomedullary junction of local medulla renal tissue, apoptotic cells of the experimental group was significantly reduced. The experiments showed that mice survived CORM-2 can be significantly reduced in mice with prolonged ischemia and reperfusion injury caused by the high mortality rate (P gt; 0.05). Conclusion carbon monoxide releasing molecule CORM-2 release CO into the blood, and also induction of HO-1 upregulation by inhibition of inflammatory cell infiltration, reduced apoptosis, thereby reducing the tubular epithelial cell necrosis, thus alleviating renal ischemia reperfusion injury.
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