Hyperbaric Oxygen Treatment Attenuates Renal Ischemia/Reperfusion Injury in Rats.

INTRODUCTION

Acute Kidney Injury (AKI) is a critical condition with high morbidity and mortality, often caused by ischemia-reperfusion (I/R) injury. Hyperbaric oxygen treatment (HBO₂) enhances tissue oxygenation and has shown potential in hypoxic conditions. This study evaluated the efficacy of HBO₂ in mitigating renal I/R injury in a rat model.

METHODS

Sprague-Dawley rats were divided into three groups: Control (sham surgery, n = 9), I/R (n = 9), and I/R +HBO (n = 9). I/R was induced by 30-minute bilateral renal pedicle occlusion followed by reperfusion. The I/R +HBO group received two sessions of HBO₂ (90 min at 1.6 ATA) at two and 22 hours post-reperfusion. Renal function was assessed via serum creatinine and blood urea nitrogen (BUN) levels. Histopathological and molecular analyses examined tissue damage, inflammation, and necroptosis markers (p-RIP3/pMLKL).

RESULTS

The I/R group showed significantly elevated BUN and creatinine levels compared to the Control (p < 0.05). HBO₂ significantly reduced these levels compared to the I/R group. Histopathology revealed severe tubular damage and neutrophil infiltration in I/R rats, while HBO₂ improved renal structure and decreased necroptosis activation.

DISCUSSION: HBO₂ effectively reduced renal I/R injury by mitigating inflammation, oxidative stress, and necroptosis. These findings suggest HBO₂ as a potential therapeutic strategy for AKI, warranting further clinical investigation.