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Ren Fail. Author manuscript; available in PMC 2017 October 01. Published in final edited form as: Ren Fail. 2016 October ; 38(9): 1476–1482. doi:10.1080/0886022X.2016.1227917.
Amelioration of Cisplatin-Induced Acute Kidney Injury by Recombinant Neutrophil Gelatinase-Associated Lipocalin Qing Ma, Shiva R. Devarajan, and Prasad Devarajan* Nephrology and Hypertension, Cincinnati Children’s Hospital Medical Center, Cincinnati, USA
Abstract Author Manuscript Author Manuscript
We investigated the protective effect and mechanism of neutrophil gelatinase-associated lipocalin (NGAL) in a murine model of cisplatin-induced nephrotoxicity. Male Swiss-Webster mice were assigned to four groups (n=10 in each group). Control mice received vehicle only. Mice in the experimental group were given a single intraperitoneal injection of cisplatin (20 mg/kg) to induce nephrotoxicity, and were divided into three groups. The first group received 100 μl of saline only via tail vein at the time of cisplatin administration. The second group was given biologically active recombinant NGAL via tail vein (250 μg/100 μl solution). The third group was injected with a 250 μg/100 μl solution of inactivated NGAL. After 4 days, we measured serum creatinine and urinary N-acetyl-β-D-glucosaminidase (NAG), and performed histologic studies. Biologically active NGAL significantly blunted the rise in serum creatinine (NGAL plus cisplatin 1.33 ± 0.31 versus cisplatin alone 2.43 ± 0.31 mg/dL, p
Ren Fail. Author manuscript; available in PMC 2017 October 01. Published in final edited form as: Ren Fail. 2016 October ; 38(9): 1476–1482. doi:10.1080/0886022X.2016.1227917.
Amelioration of Cisplatin-Induced Acute Kidney Injury by Recombinant Neutrophil Gelatinase-Associated Lipocalin Qing Ma, Shiva R. Devarajan, and Prasad Devarajan* Nephrology and Hypertension, Cincinnati Children’s Hospital Medical Center, Cincinnati, USA
Abstract Author Manuscript Author Manuscript
We investigated the protective effect and mechanism of neutrophil gelatinase-associated lipocalin (NGAL) in a murine model of cisplatin-induced nephrotoxicity. Male Swiss-Webster mice were assigned to four groups (n=10 in each group). Control mice received vehicle only. Mice in the experimental group were given a single intraperitoneal injection of cisplatin (20 mg/kg) to induce nephrotoxicity, and were divided into three groups. The first group received 100 μl of saline only via tail vein at the time of cisplatin administration. The second group was given biologically active recombinant NGAL via tail vein (250 μg/100 μl solution). The third group was injected with a 250 μg/100 μl solution of inactivated NGAL. After 4 days, we measured serum creatinine and urinary N-acetyl-β-D-glucosaminidase (NAG), and performed histologic studies. Biologically active NGAL significantly blunted the rise in serum creatinine (NGAL plus cisplatin 1.33 ± 0.31 versus cisplatin alone 2.43 ± 0.31 mg/dL, p
