Hydrogen-rich saline ameliorates the severity of l-arginine-induced acute pancreatitis in rats
Molecular hydrogen, which reacts with the hydroxyl radical, has been considered as a novel antioxidant. Here, we evaluated the protective effects of hydrogen-rich saline on the l-arginine ( l-Arg)-induced acute pancreatitis (AP). AP was induced in Sprague–Dawley rats by giving two intraperitoneal in...
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Published in | Biochemical and biophysical research communications Vol. 393; no. 2; pp. 308 - 313 |
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Main Authors | , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
05.03.2010
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Subjects | |
Online Access | Get full text |
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Summary: | Molecular hydrogen, which reacts with the hydroxyl radical, has been considered as a novel antioxidant. Here, we evaluated the protective effects of hydrogen-rich saline on the
l-arginine (
l-Arg)-induced acute pancreatitis (AP). AP was induced in Sprague–Dawley rats by giving two intraperitoneal injections of
l-Arg, each at concentrations of 250
mg/100
g body weight, with an interval of 1
h. Hydrogen-rich saline (>0.6
mM, 6
ml/kg) or saline (6
ml/kg) was administered, respectively, via tail vein 15
min after each
l-Arg administration. Severity of AP was assessed by analysis of serum amylase activity, pancreatic water content and histology. Samples of pancreas were taken for measuring malondialdehyde and myeloperoxidase. Apoptosis in pancreatic acinar cell was determined with terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling technique (TUNEL). Expression of proliferating cell nuclear antigen (PCNA) and nuclear factor kappa B (NF-κB) were detected with immunohistochemistry. Hydrogen-rich saline treatment significantly attenuated the severity of
l-Arg-induced AP by ameliorating the increased serum amylase activity, inhibiting neutrophil infiltration, lipid oxidation and pancreatic tissue edema. Moreover, hydrogen-rich saline treatment could promote acinar cell proliferation, inhibit apoptosis and NF-κB activation. These results indicate that hydrogen treatment has a protective effect against AP, and the effect is possibly due to its ability to inhibit oxidative stress, apoptosis, NF-κB activation and to promote acinar cell proliferation. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/j.bbrc.2010.02.005 |