Abstract
BackgroundContrast-induced nephropathy (CIN) is an important cause of acute renal failure. We observe the effect of rosuvastatin on preventing CIN in diabetic rats in current study.MethodsDiabetic rats were then divided into five groups: 1 diabetic rats (D), 2 diabetic rats + contrast media (DCM), 3 diabetic rats + rosuvastatin (DR), 4 diabetic rats + contrast media + rosuvastatin (DRCM), 5 non-diabetic rat control (NDCM). Contrast-induced nephropathy was induced by intravenous injection a single dose of indomethacin (10 mg/kg), double doses of N-nitro-L-arginine methyl ester (10 mg/kg) and a single dose of high-osmolar contrast medium meglumine amidotrizoate (6 ml/kg). DR and DRCM group rats were treated with rosuvastatin (10 mg/kg/day) by gavage for 5 days. At the end of treatment, the experimental groups were sacrificed, and their renal tissues were investigated histopathologically beside assessments of functional activities, nitric oxide metabolites, and oxidative stress and apoptic markers.ResultsAfter 6 days, serum creatinine and urine microprotein were increased, and creatinine clearance, kidney nitrite were decreased in DCM rats compared with NDCM, D, DR and DRCM groups. Histopathology scores in group DCM were increased compared with groups NDCM, D and DR, but lower in group DRCM than in group DCM (p < 0.01). Kidney thiobarbituric acid-reacting substances (TBARS), serum malondialdehyde (MDA), and serum protein carbonyl content (PCC) were increased, and serum thiol was decreased in the DCM group compared with groups NDCM, D and DR; however, these results were reversed in group DRCM compared with group DCM. Both expression of IL-6, TNF-α and the percentage of apoptotic cells were increased in group DCM than in groups NDCM, D and DR, but they were decreased in group DRCM than in group DCM. The expression of phospho-p38, cleaved capase-3, and the Bax/Bcl-2 ratio, were increased in group DCM than in groups NDCM, D and DR, but were decreased in group DRCM than in group DCM.ConclusionsOur study demonstrated that rosuvastatin treatment attenuated both inflammatory processes and apoptosis and inhibited oxidative stress and the p38 MAPK pathway in a diabetic rat model in the setting of CIN.
Highlights
Contrast-induced nephropathy (CIN) is one of important cause of hospital-acquired acute renal failure [1], which is associated with an increase of 25% or more, or an absolute increase of 0.5 mg/dl or more in serum creatinine from baseline value, at 48–72 h following the exposure to contrast media
Biochemical parameters Levels of serum creatinine were notably increased in the diabetic rats + contrast media (DCM) group compared with the NDCM, D or diabetic rats + rosuvastatin (DR) groups on day 6 (P < 0.01)
On day 6, creatinine clearance was notably lower in group DCM compare with groups NDCM, D, and DR (P < 0.01)
Summary
Contrast-induced nephropathy (CIN) is one of important cause of hospital-acquired acute renal failure [1], which is associated with an increase of 25% or more, or an absolute increase of 0.5 mg/dl or more in serum creatinine from baseline value, at 48–72 h following the exposure to contrast media. CIN develops more frequently after administration of contrast media in DM patients than in patients without diabetes [5]. Renal hypoxia, combined with the generation of reactive oxygen species, plays a central role in the pathogenesis of CIN, and the diabetic kidney is susceptible to intensified hypoxic and oxidative stress following the administration of contrast media [6]. The pathophysiology of this vulnerability is complex and involves various mechanisms, including a priori enhanced tubular transport activity, oxygen consumption, and the generation of reactive oxygen species [7]. We observe the effect of rosuvastatin on preventing CIN in diabetic rats in current study
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