Abstract
Oxidative stress plays an important role in the pathogenesis of acute pancreatitis (AP). As an ideal exterminator of poisonous free radicals, hydrogen can clearly reduce the degree of oxidative damage caused by severe acute pancreatitis (SAP) and lessen the presence of inflammatory cytokines. The aim of this study was to investigate the effects and mechanism of hydrogen-rich saline on SAP in rats. Serum TNF-α, IL-6, and IL-18 and histopathological score in the pancreas were reduced after hydrogen-rich saline treatment. Malondialdehyde (MDA) and myeloperoxidase (MPO) contents were obviously reduced, while superoxide dismutase (SOD) and glutathione (GSH) contents were increased after hydrogen-rich saline treatment. The expression of mRNA of tumor necrosis factor-α (TNF-α) and intercellular adhesion molecule-1 (ICAM-1) in the pancreas was reduced in hydrogen-rich saline treated group. In conclusion, intravenous hydrogen-rich saline injections could attenuate the severity of AP, probably via inhibiting the oxidative stress and reducing the presence of inflammatory mediators.
Highlights
IntroductionAttention was drawn to the role of oxygen radicals and inflammatory mediators in acute pancreatitis [1]
Acute pancreatitis (AP) is a common disease in the department of gastroenterology, but the pathogenesis of acute pancreatitis is still not fully explained
During the inflammatory response process caused by AP, insufficient blood volume, hypoxia, and discharge of large amounts of inflammatory mediators brought on by microcirculation in the pancreatic tissue will activate neutrophils and cause production of large quantities of oxygen radicals, which may heighten the degree of inflammatory response, so far as to damage internal organ function [4]
Summary
Attention was drawn to the role of oxygen radicals and inflammatory mediators in acute pancreatitis [1]. During the inflammatory response process caused by AP, insufficient blood volume, hypoxia, and discharge of large amounts of inflammatory mediators brought on by microcirculation in the pancreatic tissue will activate neutrophils and cause production of large quantities of oxygen radicals, which may heighten the degree of inflammatory response, so far as to damage internal organ function [4]. During AP, oxygen free radicals play an important role in triggering subsequential lesions in the pancreas, which were produced in damaged acinar cells as well as activated neutrophils and macrophages [8, 9]. This animal experiment was designed to study the protective effects of hydrogen-rich saline on AP in rats, for introducing a new line of thought into the treatment of SAP
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