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doi:10.1016/j.freeradbiomed.2005.02.005 
Copyright © 2005 Elsevier Inc. All rights reserved.
Original Contribution
Synergism of Helicobacter pylori infection and stress on the augmentation of gastric mucosal damage and its prevention with α-tocopherol
Tae Young Oha, 1, Marie Yeoa, 1, Sang Uk Hana, Yong Kwan Choa, Young Bae Kima, Myung Hee Chungb, Yong Seok Kima, Sung Won Choa and Ki-Baik Hahma, 
, 
Received 13 December 2004;
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Abstract
Despite evidence that Helicobacter pylori (H. pylori) infection is closely associated with stress in gastric ulcer patients, the underlying mechanism why ulcer recurrence after stress is augmented especially in patients with H. pylori remains unknown. In this study, we found that oxidative stress played a critical role in the augmented mucosal damage provoked by water immersion restraint stress (WIRS) in H. pylori infection and that an antioxidant, α-tocopherol, could ameliorate the aggravation of stress-associated gastric mucosal damage. Two hundred forty SD rats were divided into two groups according to H. pylori inoculation, and after 24 weeks of H. pylori infection, the water immersion restraint stress was imposed for 30, 120, or 480 min, respectively. To evaluate the therapeutic effects of an antioxidant, α-tocopherol was administrated 40 mg/kg daily prior to imposing WIRS. Remarkably increased hemorrhagic lesions and bleeding indexes were noted in the H. pylori-infected group with statistical significance (P < 0.05) compared to the noninfected group at the same duration of WIRS. Significantly higher oxidative stress documented by iNOS, lipid peroxides, and GSH level was detected in gastric homogenates of the H. pylori-infected group. Proteomic analysis using 2-dimensional electrophoresis showed a decrease of HSP27 and other chaperone proteins. α-Tocopherol pretreatment significantly prevented the gastric mucosal damage, caused by WIRS in the presence of H. pylori. α-Tocopherol induced HSP27 expression, which was well correlated with downregulation of iNOS mRNA. Conclusively, the presence of H. pylori caused significant deterioration of stress-induced gastric mucosal lesions through increased oxidative stress and thus antioxidant treatment such as α-tocopherol protected the gastric injuries.
Abbreviations: HSPs, heat-shock proteins; GGA, geranylgeranylacetone; SPF, specific-pathogen-free; WIRS, water immersion restraint stress; H&E, hematoxylin and eosin; TBARS, thiobarbituric acid-reactive substances; PBS, phosphate-buffered saline; Chaps, 3-[(3-cholamidopropyl)dimethylammonio]propanesulfonate; DTT, dithiothreitol; PMSF, phenylmethylsulfonyl fluoride; AGS, human gastric epithelial
Article Outline
- Introduction
- Materials and methods
- Animals
- H. pylori culture and infection
- Water immersion restraint stress
- Gross and histological observation
- TBA-reactive substance and cytokine measurement
- Two-dimensional gel electrophoresis (2-DE)
- In-gel digestion and peptide mass fingerprinting by MALDI-TOF MS
- Western blotting
- Cell culture and H. pylori infection
- Statistical assay
- Results
- The synergism of both H. pylori and stress on augmented gastric mucosal damage
- Enhancement of oxidative stress by H. pylori infection in WIRS rats
- Shift of protein profiling in augmented gastric mucosal damage of both H. pylori and stress
- The preventive effects of α-tocopherol against augmented gastric mucosal damage of WIRS in H. pylori-infected rats
- HSPs restoration by pretreatment of α-tocopherol
- Discussion
- Acknowledgements
- References
