Hydrogen-rich saline reduces the oxidative stress and relieves the severity of trauma-induced acute pancreatitis in rats

Currently, little evidence exists to support whether the therapeutic approaches for treating ordinary acute pancreatitis (AP) are effective in trauma-induced pancreatitis. Hydrogen-rich (H2) saline is an antioxidant treatment capable of ameliorating the severity of L-arginine-induced AP. In this study, we attempted to validate its protective role against traumatic pancreatitis (TP). A previously established experimental rat model of TP was generated by controlled delivery of high pressure air impact. The protective effects of H2 saline against TP were evaluated in this model system by measuring survival rate and determining changes in histopathology, plasma enzymes, cytokines, and oxidative stress-associated molecules. Intraperitoneal administration of H2-rich saline produced a pronounced protection against TP in rats. Significant improvements were observed in survival rate and histopathological findings. In addition, plasma cytokines concentrations were reduced in H2 saline-treated TP rats. Although no marked inhibitory effect on plasma amylase and lipase activities was observed, H2 saline caused considerable suppression of pancreatic malondialdehyde level and recruitment of endogenous pancreatic antioxidants, such as glutathione and superoxide dismutase. H2-rich saline has beneficial effects on TP, presumably because of its detoxification activities against excessive reactive oxygen species. Our findings highlight the potential of H2-rich saline as a therapeutic agent of trauma-induced AP.

Pre-inhalation of hydrogen-rich gases protect against caerulein-induced mouse acute pancreatitis while enhance the pancreatic Hsp60 protein expression

Background: Acute pancreatitis (AP) lacks targeted prevention and treatment measures. Some key points in the pathogenesis of AP remain unclear, such as early activation of pancreatic enzymes. Several recent reports have shown the protective effect of hydrogen on several AP animal models, and the mechanism is related to antioxidant activity. Heat shock protein 60 (Hsp60) is known to accompany pancreatic enzymes synthesis and secretion pathway of in pancreatic acinar cells, while role of hsp60 in AP remains a topic. Aim of this study was to investigate effect of hydrogen pretreatment on AP and the mechanisms, focusing on pancreatic oxidative stress and Hsp60 expression. Methods: 80 mice were randomly assigned into four groups: HAP group, AP group, HNS group, and NS group and each group were set 3 observation time point as 1 h, 3 h and 5 h (n = 6-8). Mouse AP model was induced by intraperitoneal injection of 50 μg/kg caerulein per hour for 6 injections both in AP and HAP groups, and mice in NS group and HNS group given normal saline (NS) injections at the same way as control respectively. Mice in HAP group and HNS group were treated with hydrogen-rich gases inhalation for 3 days before the first injection of caerulein or saline, while mice in AP group and NS group in normal air condition. Histopathology of pancreatic tissue, plasma amylase and lipase, plasma IL-1 and IL-6, pancreatic glutathione (GSH) and malondialdehyde (MDA), and Hsp60 mRNA and protein expression were investigated. Comparisons were made by one-way analysis of variance. Results: The pancreatic pathological changes, plasma amylase and lipase activity, and the increase of plasma IL-1 and IL-6 levels in AP mice were significantly improved by the hydrogen-rich gases pretreatment, Meanwhile, the pancreatic GSH content increased and the pancreatic MDA content decreased. And, the hydrogen-rich gases pretreatment improved the Hsp60 protein expression in pancreatic tissues of AP mice at 1 h and 5 h. Conclusions: Pre-inhalation of hydrogen-rich gases have a good protective effect on AP mice, and the possible mechanisms of reduced oxidative stress and the early increased pancreatic Hsp60 protein deserve attention.