Renal Protective Effect of Probucol in Rats with Contrast-Induced Nephropathy and its Underlying Mechanism

Abstract

BackgroundContrast-induced nephropathy (CIN) refers to acute renal damage that occurs after the use of contrast agents. This study investigated the renal protective effect of probucol in a rat model of contrast-induced nephropathy and the mechanism of its effect.Material/MethodsTwenty-eight Wistar rats were randomly divided into the control group, model group, N-acetylcysteine(NAC) group, and probucol group. We used a rat model of iopromide-induced CIN. One day prior to modeling, the rats received gavage. At 24 h after the modeling, blood biochemistry and urine protein were assessed. Malondialdehyde (MDA) and superoxide dismutase (SOD) were measured in renal tissue. Kidney sections were created for histopathological examination.ResultsThe model group of rats showed significantly elevated levels of blood creatinine, urea nitrogen, 24-h urine protein, histopathological scores, and parameters of oxidative stress (P<0.05). Both the NAC and probucol groups demonstrated significantly lower Scr, BUN, and urine protein levels compared to the model group (P<0.05), with no significant difference between these 2 groups. The NAC group and the probucol group had significantly lower MDA and higher SOD than the model group at 24 h after modeling (P<0.05). The 8-OHdG-positive tubule of the probucol group and NAC group were significantly lower than those of the model group (p=0.046, P=0.0008), with significant difference between these 2 groups (P=0.024).ConclusionsProbucol can effectively reduce kidney damage caused by contrast agent. The underlying mechanism may be that probucol accelerates the recovery of renal function and renal pathology by reducing local renal oxidative stress.

Nephroprotective Effects of N‐Acetylcysteine Amide against Contrast‐Induced Nephropathy through Upregulating Thioredoxin‐1, Inhibiting ASK1/p38MAPK Pathway, and Suppressing Oxidative Stress and Apoptosis in Rats

“…The oxidative stress induced in rats with CIN was evident by drastically decreased levels of SOD and GSH, as well as an increased level of MDA, which is consistent with our previous data [6, 7] and other reports [34, 35]. The findings that NACA consistently exhibited better renoprotection than NAC may be related to its better membrane penetration.…”

“…Since there is significant inconsistency in the guidelines regarding the benefit of NAC to reduce the risk for CIN [1, 35], large-scale, randomized clinical trials that are adequately powered have been proposed to determine the effectiveness of NAC for prevention of CIN. Our present findings suggest that consideration should be given to the use of NACA as a result of its superior renoprotective function relative to NAC.…”

Characterization of Polysaccharides Extracted from Sargassum fusiforme and Its Effective Prevention of Contrast-Induced Nephropathy via Enhancing Antioxidant Capacity

“…Sham and CIN rats were given saline. After pretreatment with cSFP-C or saline, CIN was developed in CIN and CIN+cSFP-C rats on the basis of previously described reports [28]. Briefly, under pentobarbital sodium anesthesia, rats were given 10 mg/kg indomethacin, followed 10 mg/kg NW-nitro-Larginine methyl ester (L-NAME) 15 min later and 1600 mg iodine/kg of iopromide 30 min later.…”

The Diagnostic Value of HIF-2 Alpha to Determine The Development and Efficacy of Treatment for Contrast Induced Nephropathy: An Experimental Study

“…In recent years, along with the fast development in medical imaging techniques, the examinations and treatments with intravenous contrast agents in emergency services or other services may induce CIN. CIN is one the most important causes of acute renal damage/injury in patients followed at emergency services and inpatients [2]- [4]. In the current literature, the rates for CIN was reported between 0.2-2.0%, after tomography undertaken with contrast agents [1].…”

“…Pathophysiologically, CIN is closely related with renal hemodynamic changes, medullar ischemic injury, oxidative stress injury formed with reactive oxygen species (ROS), secondary damage to tubules and tubular obstruction [5]. In many experimental 3 / 23 studies, chronic hypoxic damage is pointed out as an eventual common way to cause the progression of chronic renal disease (CRD) to end-stage renal failure [2]. Thus, the therapeutic intervention to hypoxia may be a valid tool to cease the CRD.…”