Exploring the Impact of Contrast-Induced Nephropathy on NRF2 Expression in Renal Tissues of Wistar Rats: A Pathway to Oxidative Stress Modulation
DOI:
https://doi.org/10.70135/seejph.vi.4826Abstract
Introduction: Contrast-Induced Nephropathy (CIN) is a form of acute kidney injury that arises following the administration of intravascular contrast agents. The increasing use of contrast agents in medical practice raises the incidence of CIN, which is associated with complications, prolonged hospitalization, and increased mortality. Nuclear Factor Erythroid Related Factor-2 (NRF2) plays a critical role in antioxidant and anti-inflammatory responses, making it a potential therapeutic target to mitigate CIN.
Objectives: This study aimed to evaluate the temporal changes in NRF2 expression in renal tissues following contrast media administration in a rat model.
Methods: Twenty-four male Wistar rats (Rattus norvegicus), aged 2-3 months, were divided into four groups: one control group and three intervention groups, which received Iopromide (370 mg iodine/mL) at a dose of 1600 mg iodine/kg body weight. NRF2 expression was assessed by immunohistochemistry using H-Score analysis, which quantifies the intensity and percentage of positive cells in glomeruli, tubules, and intrarenal vasculature, at 24, 48, and 72 hours post-injection. Statistical analysis was performed using SPSS, including homogeneity and normality tests, followed by one-way ANOVA and LSD post hoc tests.
Results: NRF2 expression showed no significant change in the glomerulus and intrarenal vasculature (p = 0.660 and p = 0.075, respectively). NRF2 expression in the renal tubules exhibited significant differences (p < 0.001) at 24 and 48 hours, but returned to baseline at 72 hours (p = 0.902).
Conclusions: NRF2 expression remained stable in the glomerulus and intrarenal vasculature, while renal tubule NRF2 expression increased significantly at 24 and 48 hours, suggesting a potential early protective response. These findings highlight the temporal dynamics of NRF2 activation and its potential therapeutic implications in preventing CIN.
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