#207 Early single session of hyperbaric oxygen therapy mitigates renal apoptosis in lipopolysaccharides-induced endotoxemia in rats

Background and Aims Sepsis-associated acute kidney injury (SA-AKI) is a prominent sepsis complication, often having adverse clinical outcomes. Hyperbaric oxygen therapy (HBOT), known for its anti-inflammatory characteristics, antioxidant effects, and ability to deliver high oxygen tension to hypo-perfused tissues, may offer potential benefits for SA-AKI. This study investigated whether HBOT improved renal injury in sepsis and elucidated its underlying mechanisms. Method An lipopolysaccharides (LPS)-induced endotoxemia model was established using eight-week-old C57BL/6 mice. Thirty minutes post-LPS administration, a subset of mice underwent HBOT at a 2.5 atmospheric pressure absolute with 100% oxygen for 60 minutes. After 24 hours, all mice were euthanized for measurements. Results Our results demonstrated that HBOT effectively mitigated renal tubular cell apoptosis, as evidenced by decreased apoptosis-associated proteins, including Bax/Bcl-2 and cleaved caspase 3/caspase 3 ratios. HBOT significantly reduced phosphorylated p53 proteins and cytochrome C levels, suggesting that HBOT may attenuate renal apoptosis through decreased p53 activation and cytochrome C release. Notably, HBOT preserved manganese-dependent levels of superoxide dismutase, an antioxidant enzyme, compared to the LPS group. Furthermore, transforming growth factor-β (TGF- β)/Smad4 and alpha-smooth muscle actin expressions were significantly reduced in the LPS+HBOT group. Conclusion An early single session of HBOT exhibited renoprotective effects in LPS-induced endotoxemia mice models by mitigating apoptosis by suppressing p53 activation and cytochrome C levels. The observed TGF-β decrease, downstream Smad expression reduction, and antioxidant capacity preservation following HBOT may contribute to these effects.