Gallic acid, renal redox balance and NRF2-Related transcript-level modulation in a rat model of contrast-associated acute kidney injury.

INTRODUCTION

Contrast-associated acute kidney injury (CA-AKI) is a clinically relevant complication of iodinated contrast exposure. This study investigated whether gallic acid (GA) attenuates diatrizoate (Urografin 76%; URO)-induced renal injury in rats and whether this effect is associated with nuclear factor erythroid 2-related factor 2 (NRF2)/Kelch-like ECH-associated protein 1 (Keap-1)/heme oxygenase-1 (HO-1) transcript-level changes.

METHODS

Thirty-two female Wistar rats were randomized into Control, URO, URO + GA, and GA groups (n = 8/group). GA was administered intraperitoneally at 100 mg/kg 15 min before URO. At 24 h, serum urea and creatinine, renal total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), histopathology, tumor necrosis factor-alpha (TNF-alpha) and caspase-3 immunohistochemistry, and NRF2/Keap-1/HO-1 mRNA expression were evaluated.

RESULTS

URO significantly increased serum urea and creatinine and induced renal oxidative imbalance, as shown by increased TOS and OSI and reduced TAS. GA co-treatment significantly decreased TOS and OSI and partially restored TAS, whereas urea and creatinine showed only non-significant downward trends. Histopathologically, GA attenuated collagenous material accumulation, while other acute tubular injury parameters were not significantly improved. TNF-alpha and caspase-3 immunoreactivity remained weak/focal without significant intergroup differences. URO reduced NRF2, Keap-1, and HO-1 mRNA levels, whereas GA restored these transcripts toward control values.

CONCLUSION

GA was associated with biochemical and transcript-level attenuation of acute diatrizoate-induced CA-AKI, mainly through improved renal redox balance and restoration of NRF2-related transcripts. However, functional renoprotection and NRF2 pathway activation were not definitively demonstrated.