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Volume 39 (2006)
- Issue 3 Pages 103-
- Issue 2 Pages 55-
- Issue 1 Pages 1-
Volume 39, Issue 2
Displaying 1-7 of 7 articles from this issue
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Serial Reviews
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Yuji Naito2006 Volume 39 Issue 2 Pages 55
Published: 2006
Released on J-STAGE: August 24, 2006
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Hidekazu Suzuki, Toshifumi Hibi2006 Volume 39 Issue 2 Pages 56-63
Published: 2006
Released on J-STAGE: August 24, 2006
JOURNAL FREE ACCESSHelicobacter pylori (H. pylori) is a spiral-shaped, Gram-negative rod, which induces the infiltration to the gastric mucosa by neutrophils, macrophages, and T and B lymphocytes; however, this immune and inflammatory response cannot completely clear the bacterial infection, and leaves the host prone to complications resulting from persistent inflammation. Resultantly, H. pylori infection causes chronic inflammation, accumulation of reactive oxygen species, and oxidative DNA damage in the gastric mucosa. Recent studies reveal that H. pylori injects bacterial proteins into the cytosol of the gastric host cell via the type IV injection system and regulates the intracellular signal transduction [1, 2]. This mechanism provides a novel means of resolving how H. pylori survives in the acidic environment of the human stomach. During persistent gastric infections, chronic gastritis may remain asymptomatic or may evolve into more severe diseases, such as peptic ulcer disease or atrophic gastritis. In addition, infection with H. pylori increases the risk of developing gastric cancer and mucosa-associated lymphoid tissue lymphoma. Various gastric diseases, such as gastritis, ulcers, intestinal metaplasia, and gastric cancer, can be appropriately developed by inoculating this bacteria into Mongolian gerbils [3]. In addition, the successful eradication of H. pylori is useful as a preventive approach against gastric cancer [4]. This review focuses on the aspects of the oxidative mechanism in the H. pylori-associated gastric mucosal lesion formation.
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Original Articles
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Sachiko Hachiya, Yasuhide Okuhara, Violeta Raneva, Norihiro Shigematsu2006 Volume 39 Issue 2 Pages 64-68
Published: 2006
Released on J-STAGE: August 24, 2006
JOURNAL FREE ACCESSWe examined the effect of difructose anhydride III (DFAIII) on zinc absorption in rats in two experiments. First, we compared the absorption of zinc from zinc gluconate and zinc yeast with or without DFAIII by measuring concentrations in plasma collected from the portal vein after a single oral administration of zinc gluconate or zinc yeast with or without DFAIII. The peak plasma zinc concentration and the incremental area under the curve (IAUC) of plasma zinc 6 h after administration were highest in the zinc gluconate with DFAIII group. Second, we examined the effect of DFAIII on the absorption of zinc with phytic acid. with or without DFAIII. Plasma zinc levels in groups both with and without DFAIII were nearly the same as those at the baseline. Our results showed that DFAIII was better with zinc gluconate than zinc yeast for zinc absorption, and that DFAIII does not alter the inhibitory effects of phytic acid on zinc absorption.
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Hiroshi Ichikawa, Norimasa Yoshida, Tomohisa Takagi, Osamu Handa, Yuji ...2006 Volume 39 Issue 2 Pages 69-74
Published: 2006
Released on J-STAGE: August 24, 2006
JOURNAL FREE ACCESSNeutrophils activation and inflammatory cytokines play a critical role in aspirin-induced gastric mucosal injury. FR167653 was first discovered to be a potent inhibitor of interleukin (IL)-1β and tumor necrosis factor-α (TNF-α) production. The purpose of this study is to investigate the anti-inflammatory effects against aspirin-induced gastric mucosal injury in rats. The intragastric administration of acidified aspirin induced hyperemia and hemorrhagic erosions in rat stomachs. The increase in the total gastric erosive area after aspirin administration was significantly inhibited by treatment with FR167653 in a dose-dependent manner. The increases in thiobarbituric acid-reactive substances, myeloperoxidase activity and the contents of TNF-α and IL-1β in gastric mucosa after aspirin administration were both significantly inhibited by pre-treatment with FR167653. Based on these data, the beneficial effects of FR167653 on aspirin-induced gastric mucosal injury may be attributed to its anti-inflammatory properties.
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Jai C. Tilak, Thomas P.A. Devasagayam, Soumyakanti Adhikari, Ramachand ...2006 Volume 39 Issue 2 Pages 75-87
Published: 2006
Released on J-STAGE: August 24, 2006
JOURNAL FREE ACCESSTerminalia arjuna (T. arjuna) is an Indian medicinal plant credited with cardiotonic and cardioprotective properties; and baicalein is the active ingredient. To determine the possible mechanisms of protective action of T. arjuna and baicalein, we studied the reactions of T. arjuna extracts and baicalein with the biologically important superoxide (O2·−) and singlet oxygen (1O2) by measuring O2·− or 1O2 induced damage of lipids, lipid preoxidation, in the reaction mixture containing rat liver mitochondria and cardiac homogenate. Absorption of T. arjuna and baicalein in rat small intestine was also assessed. In addition, inhibitory effect of T. arjuna and baicalein on radiation-induced ROS generation in NIH3T3 cells and a cell-free chemical system, as well as on whole plasma oxidation were studied. Significant absorption of T. arjuna and baicalein from the intestine was observed. Baicalein is highly effective in inhibiting lipid peroxidation, reactive oxygen species generation, and plasma oxidation, even at low concentrations of 10-25 μM. To determine the possible mechanisms in this phenomena, we studied the reaction of T. arjuna extracts and baicalein with O2·− and 1O2 using electron spin resonance and found that T. arjuna extracts and baicalein possess higher scavenging activities than that of standard antioxidants; 50% Inhibitory concentration (IC50) of the aqueous extract of T. arjuna is 0.6 × 10−3 and 22.5 × 10−3% (w/v) and IC50 of baicalein for O2·− is 18 μM, while IC50 for 1O2 is 129 μM. Pulse radiolysis study with baicalein shows that the bimolecular rate constant between baicalein and O2·− is 1 × 108 M−1s−1. In conclusion, our results show that T. arjuna and baicalein are very potent in membrane protection against O2·− and 1O2 in vitro, and their ability to react with these species may explain previously observed effects of this plant and its active ingredient.
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Kiyoshi Yokoyama, Noriko Nakajima, Yoko Ito, Ariyoshi Iwasaki, Yasuyuk ...2006 Volume 39 Issue 2 Pages 88-97
Published: 2006
Released on J-STAGE: August 24, 2006
JOURNAL FREE ACCESSInflammatory bowel disease (IBD) is a chronic disease of the digestive tract, with complicated and multifactoral etiology. An exaggerated intestinal immune response to otherwise innocuous stimuli plays a key role in the pathophysiology of this intestinal disorder. Nutritional intervention is an important therapy for patients with IBD. But the ratio of n-3 and n-6 fatty acids on the modulation of intestinal inflammation is not clear. Interleukin-16 (IL-16) is a pleiotrophic cytokine secreted mainly by CD8+ T cells. The properties of IL-16 suggest that it may be involved in pathophysiological process of chronic inflammatory diseases. The aim was to determine the effect of an n-3 fatty acid-rich diet (RACOL®) on the expressions of cytokines and mucosal integrity in trinitrobenzene surufonic acid (TNBS) induced rat colitis. 7 week-male Wistar rats were divided into 4 groups. 1. Normal laboratory diet (n = 10), 2. RACOL® diet only (n = 10), 3. TNBS induced colitis with normal laboratory diet (n = 10), 4. TNBS induced colitis with RACOL® diet (n = 10). TNBS induced colitis rats were given an intracolonic injection of 50 mg of TNBS dissolved in 50% ethanol. From day 2, rats were fed 80 kcal/day of RACOL® and/or normal laboratory diet, and sacrified on the 14th and the 28th days. One hour before sacrifice, 0.2 mg/g/rat of BrdU was injected. The expressions of BrdU labeled cells, tumor necrosis factor (TNF)-α, interferon (IFN)-γ and IL-16 were studied by the ABC staining method and DAB staining lesions in colonic mucosa were estimated by an image analyzer system. Apoptosis was assessed by the TUNEL method. Macroscopic and histological findings were classified by the Morris and Vilaseca method. TNBS application increased colonic epithelial cell proliferation, but nutrition by RACOL® reduced this stimulation. Number of apoptosis cells was also increased by TNBS application, but nutrition of RACOL® reduced the number of apoptosis cells, which had been increased by TNBS treatment. The expressions of cytokines had been increased in TNBS-colitis rats, but were reduced by the RACOL®. In conclusion, the effect of nutrition by n-3 fatty acid-rich diet, RACOL®, is an important treatment through the inhibition of inflammatory mediators, and colonic hyper-proliferation.
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Tomiyasu Arisawa, Tomomitsu Tahara, Tomoyuki Shibata, Mitsuo Nagasaka, ...2006 Volume 39 Issue 2 Pages 98-101
Published: 2006
Released on J-STAGE: August 24, 2006
JOURNAL FREE ACCESSTrypsin acting at protease-activated receptor 2 (PAR2) has been reported to contribute to a progression of malignant tumors. In addition, a polymorphic form of PAR2 has been also reported to display reduced sensitivity to trypsin. However, a frequency of PAR2 polymorphism is unknown in Japan. The aim of the present study was to clarify a frequency of PAR2 polymorphism in Japan and to evaluate the relation between this polymorphism and gastric cancer. We estimated PAR2 T719C in 106 patients with gastric cancer (GC cases) and 96 patients without gastric cancer (non-GC cases). We employed a single-strand conformation polymorphism analysis after polymerase chain reaction (PCR-SSCP) for detecting of this polymorphism. There was no significant difference between GC and non-GC cases in the distribution of gender (M:F = 2.66 and 2.00, respectively) and age (mean age = 66.12 and 63.50, respectively). Helicobacter pylori (H. pylori) positive ratio was 81.7% (GC cases: 92.0%, non-GC cases: 72.5%, p<0.01). Single strand bands of 719C were not detected in all 202 patients by PCR-SSCP. In conclusion, a polymorphism F240S of PAR2 is very rare and does not contribute to the genesis and progression of gastric cancer in Japanese population.
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