hyperbaric oxygen therapy suppresses apoptosis and promotes renal tubular regeneration after renal ischemia/reperfusion injury in rats

results a significant decrease in apoptotic cells and increase in proliferative reaction were observed in the i/r + hbo group compared to the i/r group. conclusions we demonstrated that hbo suppressed apoptosis, which caused inflammation after renal i/r, and promoted tubular cell regeneration. hbo has protective effects against aki caused by renal i/r through the inhibition of apoptosis. materials and methods sprague-dawley (sd) rats were randomized into three groups: sham (sham-operated rats); i/r (animals submitted to i/r); and i/r + hbo (i/r rats exposed to hbo). tubular cell apoptosis was confirmed by dna laddering and the terminal deoxynucleotidyl transferase-mediated uridine triphosphate nick end labeling (tunel) assay. cellular proliferation activity was determined using the anti-ki-67 antibody. objectives we studied the possible beneficial effects of hbo therapy on apoptosis and tubular cell regeneration after renal i/r injury in rats. background renal ischemia/reperfusion (i/r) injury remains a major cause of acute kidney injury (aki), in addition to i/r injury-induced tissue inflammation, necrosis and apoptosis. hyperbaric oxygen therapy (hbo) is defined as a treatment in which a patient is intermittently exposed to 100% oxygen pressurized to a pressure above sea level (> 2.0 atmospheres absolute (ata), 1.0 ata = 760 mmhg). it has been used in a number of medical conditions with a proven efficacy in a limited number of disorders. however, the effects of hbo therapy on apoptosis and proliferative activity after i/r injury have not been fully understood.