Abstract: Objective To investigate the effect of hydrogen-rich saline (HRS) on endotoxin (LPS)-induced pancreatic injury in mice with sepsis and its possible mechanism. Methods The mouse model of pancreatic injury of sepsis was established by tail intravenous injection of LPS. Male C57BL/6J mice were randomly divided into 3 groups with 6 mice in each group. They were control group, model/LPS group (LPS 5 mg/kg tail vein injection) and HRS treatment/LPS+HRS group (HRS 10 mL/kg intraperitoneal injection 1 h after LPS modeling). After modeling, the behavioral manifestations were observed in three groups of mice. After 24 h, pancreatic tissue was stained with hematoxylin eosin (HE), and the modified Schmidt pancreas histopathological score was performed under microscope. The serum amylase, levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6, myeloperoxidase (MPO) and malonaldehyde (MDA) in the pancreatic tissues were detected by enzyme-linked immunosorbent assay (ELISA). Results Compared with the control group, mice in the LPS group showed drowsiness, shivering, slow movement, less grooming activities and severe diarrhea. There were occurred edema, inflammatory cell infiltration, hemorrhage and necrosis in pancreatic tissues. The modified Schmidt histopathologic score increased. The serum amylase level increased, and TNF-α, IL-6, MPO and MDA levels in pancreatic tissues were also increased (P＜0.05). Compared with the LPS group, the drowsiness and shivering were reduced, the combing activity was increased and diarrhea was alleviated with less excreta in the LPS+HRS group. The edema, inflammatory cell infiltration, hemorrhage and necrosis in pancreatic tissues were reduced in mice. There were no significant changes in the modified Schmidt histopathology scores between the two groups (P＞0.05). The serum amylase level, and TNF-α, IL-6, MPO and MDA levels in the pancreas were significantly decreased, but which were still higher than those of control group (P＜0.05). Conclusion HRS can significantly improve LPS-induced septic pancreatic injury in mice by inhibiting inflammatory response and alleviating oxidative stress.

Key words: sepsis, pancreatic diseases, oxidative stress, inflammation, hydrogen-rich saline, pancreatic injury