Hyperbaric Oxygen Reduces Inflammatory Response in Acute Pancreatitis by Inhibiting NF-κB Activation

Abstract

Aim: The mechanism of hyperbaric oxygen (HBO) therapy for acute pancreatitis has not been fully clarified yet. The main purpose of this study was to investigate the effect of HBO on nuclear factor κB (NF-κB) activation and the inflammatory response in rats with acute necrotizing pancreatitis (ANP). Methods: A total of 120 male Sprague-Dawley rats were randomly divided into 3 groups (40 in each): control, ANP and ANP + HBO. ANP rat models were established by a retrograde injection of 5% sodium taurocholate into the pancreatic duct. HBO treatment was performed at 2.5-fold absolute atmospheric pressure in 90% oxygen for 1, 3, 5, and 7 h. The activation of NF-κB and its inhibitor IκBα in peripheral blood neutrophilic granulocytes was measured by electrophoretic mobility shift assay and Western blot, respectively. The inflammatory cytokines [interleukin (IL)-2, IL-6, tumor necrosis factor-α (TNF-α), and intercellular adhesion molecule 1] in the blood were measured by enzyme-linked immunosorbent assay. Results: The blood levels of inflammatory cytokines and NF-κB activation were significantly increased in ANP rats compared to control rats, but IκBα activation was suppressed. The levels of the elevated inflammatory cytokines were positively correlated with the changes in NF-κB activation. After HBO treatment, the blood levels of inflammatory cytokines and NF-κB activation were significantly decreased in the ANP + HBO group in a time-dependent manner, but IκBα activation was increased. Conclusion: Our findings suggest that acute pancreatitis is associated with the upregulation of cytokines in blood as well as upregulation of NF-κB levels and downregulation of IκBα activation in peripheral blood neutrophilic granulocytes. In contrast, HBO plays a role in acute pancreatitis treatment by normalizing these changes.