Hydrogen-rich saline ameliorates the severity of L-arginine-induced acute pancreatitis in rats
Creators
- 1. Department of General Surgery, Shanghai Chang Zheng Hospital, Second Military Medical University, Shanghai 200003 (China)
- 2. Department of Diving Medicine, Faculty of Naval Medicine, Second Military Medical University, Shanghai 200433 (China)
- 3. Department of Clinical Laboratory, Shanghai East Hospital, Tong Ji University, Shanghai 200120 (China)
Description
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.
Availability note (English)
Available from http://dx.doi.org/10.1016/j.bbrc.2010.02.005Additional details
Identifiers
- DOI
- 10.1016/j.bbrc.2010.02.005;
- PII
- S0006-291X(10)00197-X;
Publishing Information
- Journal Title
- Biochemical and Biophysical Research Communications
- Journal Volume
- 393
- Journal Issue
- 2
- Journal Page Range
- p. 308-313
- ISSN
- 0006-291X
- CODEN
- BBRCA9
INIS
- Country of Publication
- United States
- Country of Input or Organization
- International Atomic Energy Agency (IAEA)
- INIS RN
- 45023310
- Subject category
- S60: APPLIED LIFE SCIENCES;
- Descriptors DEI
- AMYLASE; ANIMAL TISSUES; ANTIOXIDANTS; APOPTOSIS; ARGININE; CELL PROLIFERATION; CONCENTRATION RATIO; DEOXYURIDINE; DIGESTIVE SYSTEM DISEASES; EDEMA; HYDROXYL RADICALS; INTRAPERITONEAL INJECTION; LIPIDS; NEUTROPHILS; OXIDATION; PANCREAS; RATS; VEINS
- Descriptors DEC
- AMINO ACIDS; ANIMALS; ANTIMETABOLITES; AZINES; BIOLOGICAL MATERIALS; BLOOD; BLOOD CELLS; BLOOD VESSELS; BODY; BODY FLUIDS; CARBOXYLIC ACIDS; CARDIOVASCULAR SYSTEM; CHEMICAL REACTIONS; DIGESTIVE SYSTEM; DIMENSIONLESS NUMBERS; DISEASES; DRUGS; ENDOCRINE GLANDS; ENZYMES; GLANDS; GLYCOSYL HYDROLASES; HETEROCYCLIC COMPOUNDS; HYDROLASES; HYDROXY COMPOUNDS; INJECTION; INTAKE; LEUKOCYTES; MAMMALS; MATERIALS; NUCLEOSIDES; NUCLEOTIDES; O-GLYCOSYL HYDROLASES; ORGANIC ACIDS; ORGANIC COMPOUNDS; ORGANIC NITROGEN COMPOUNDS; ORGANS; PATHOLOGICAL CHANGES; PROTEINS; PYRIMIDINES; RADICALS; RIBOSIDES; RODENTS; SYMPTOMS; URACILS; VERTEBRATES
Optional Information
- Copyright
- Copyright (c) 2010 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.