• The Korean Journal of Nuclear Medicine
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• v.23 no.1
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• pp.41-48
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• 1989

$^{99m}Tc-Pertechnetate\;(TcO_4^-)$ is concentrated by the stomach after intravenous injection, allowing the detection of ectopic gastric mucosa. It has been used to develop a noninvasive test of gastric secretion. However the cellular site of concentration is still controversial, that is whether mucin-secreting epithelial cell or acid-secreting parietal cell. This study is planned to investigate the effects of cimetidine and gastric acidity on the retention of $TcO_4^-$ in the gastric wall of the rat. Also we further attempted to clarify the uptake and secreting cell of $TcO_4^-$ in the gastric mucosa. One hundred rats were divided into two groups, preliminary (40 rats) and main examination group (60 rats). Preliminary examination group was composed of fasting group (20 rats) for the detection of the time for reaching stable $TcO_4^-$ retention ratio in gastric wall and post-prandial group (20 rats) for the detection of the time for reaching the maximal gastric acidity. Main examination group was composed of fasting group (30 rats), which was subdivided into control group (10 rats), cimetidine group (10rats), $Mylanta^{(R)}$ group (10 rats) and post?prandial group (30 rats), which was subaivided into 90 min group (10 rats), 90 min cimetidine group (10 rats), and 120 min group (10 rats). Retention ratio (%) of $TcO_4$ in the gastric wall and the pH of the gastric contents were measured in the extracted stomach of the six groups. Gastric wall retention ratio of $TcO_4^-$ was calculated by the gastric wall radioactivity (cpm) divided by total gastric radioactivity (cpm) at 30 mins after intravenous injection of 0.4 mCi of $TcO_4^-$. The results were as follows: 1) The time required for reaching stable $TcO_4$ retention ratio and the lowest gastric PH were 30 min and 90 min, respectively. 2) In the fasting group, the gastric wall retention ratio of $TcO_4^-$ was significantly increased in the cimetidine group, compared with the control group (P < 0.01). However there was no significant difference between the control and $Mylanta^{(R)}$ group 3) The $TcO_4^-$ retention ratios of 90 min and 120 min groups were lower than that of the fasting control group (p < 0.05), either. After administration of cimetidine, the retention ratio was significantly increased in 90 min group (p < 0.01). 4) While $TcO_4^-$ retention ratio and gastric pH were well correlated in the post-prandial 120 min group (r=0.7112, p<0.05), in the post-prandial 90 min and 90 min cimetidine groups correlated poorly. However, there was no correlation in the three fasting groups at all. Referring the above results, we infer that $TcO_4^-$ is secreted into the gastric lumen by both parietal and non-parietal cells, with dominant non-parietal $TcO_4^-$ secretion in the fasting state and dominant parietal $TcO_4^-$ secretion in the stimulated state.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.11 no.sup1
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• pp.83-92
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• 2008

Helicobacter pylori is the causative agent of chronic gastritis and has a role in the pathogenesis of peptic ulcer diseases, and gastric cancer. There have been reports suggesting a close link between these gastroduodenal disorders and a state of vitamin C deficiency. In this paper, the past, present and future perspectives on H. pylori infection and vitamin C will be discussed under the following view points. Since the ecological niche of H. pylori is the mucus layer and intercellular junctions of the gastric epithelium, the various kinds of host inflammatory cells motivated by the local and systemic immune responses cannot eliminate the microorganisms. When the invading foreign body is not removed, despite full activation of defense mechanisms, adverse consequences of the immune responses develop on the host gastric mucosa. The reasons for the body vitamin C depletion could be explained as follows; 1) the increased vitamin C consumption by increased oxygen free radical production through the prolonged hypersensitivity reactions in the gastric mucosa, 2) the increased vitamin C oxidation by the nitrite which is formed from nitrate reduction by the intragastric bacteria proliferated in the hypochlorhydric gastric cavity, 3) the strong ${\gamma}$-glutamyltranspeptidase activity of H. pylori which depletes the glutathiones in gastric mucosa. Depletion of glutathiones in the stomach favors irreversible oxidative destruction of ascorbic acid. Both persistent inflammatory burdens in the stomach by H. pylori and resultant vitamin C depletions synergistically and uninhibitedly might aggravate the hypothetical sequence of gastric carcinogenesis: atrophic gastritis${\rightarrow}$intestinal metaplasia${\rightarrow}$dysplasia${\rightarrow}$gastric adenocarcinoma. High intake of vitamin C could reverse the hypothetical sequence of the gastric carcinogenesis via direct and indirect effects on H. pylori and host-parasite relationships.

• Journal of Gastric Cancer
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• v.4 no.3
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• pp.149-155
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• 2004

Purpose: According to the recent studies, it is shown that the polymorphism of Interleukin $1\beta$ gene is associated with the incidence of gastric cancer caused by the Helicobacter pylori infection. Interleukin $1\beta$ is a cytokine markedly inhibiting gastric acid secretion. Interleukin $1\beta$ production associated with Helicobacter pylori gastric infection may exacerbate mucosal damage including chronic gastritis and atrophic gastritis, may induce eventual neoplasia. Among these Interleukin $1\beta$ gene polymorphisms, polymorphisms at -31 portion and -511 portion may associated with these processes, eventually increase the risk of gastric cancer. We investigated the risk of gastric cancer according to the Helicobacter pylori infection and genetic polymorphism of Interleukin $1\beta$ in gastric cancer patients. Materials and Methods: 176 individuals with gastric cancer and 40 healthy controls were analyzed. Each group was divided into two groups whether they infected with Helicobacter pylori or not. DNA was extracted from the peripheral blood in all groups. The PCR-RFLP method was used for investigating the distribution of genotype of C/C, C/T, T/T at -31 portion and -511 portion. Results: T/T genotype at -511 portion was $19.3\%$ in gastric cancer cases and $10\%$ in controls, which was statistically significant. (P=0.0432) The risk of gastric cancer was increased 4.86 ($1.26\∼18.77$) in group which had T/T genotype. In gastric cancer cases, C/C genotype at 31 portion was $27.6\%$ in group with Helicobacter pylori infection and $12.8\%$ in group without infection, which was statistically significant. (P=0.0047) The risk of gastric cancer was increased 4.82 ($1.81\~12.81$) in group which had C/C genotype. Conclusion: T genotype at -511 portion among the Interleukin $1\beta$ genetic polymorphisms may be the risk factor of gastric cancer. And, with Helicobacter pylori infection, C genotype at -31 portion may be the risk factor of gastric cancer.

• The Korean Journal of Pharmacology
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• v.23 no.2
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• pp.87-94
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• 1987

The role of central adrenergic activity in the genesis of stress ulcers was investigated by intracerebroventricular (i.c.v.) administration of catecholamines and clonidine in pylorus-ligated rats restrained for 4 hours at a temperature of $4^{\circ}C$. 1. The stress-induced ulceration was markedly decreased by the i.c.v. administration of norepinephrine, epinephrine, dopamine or low dose of clonidine. 2. After an i.c.v. administration of norepinephrine or epinephrine, the volume of gastric juice, and both acid and pepsin secretion were markedly decreased. 3. Dopamine or a low dose of clonidne decreased the volume of gastric juice and acid secretion but did not affect pepsin secretion. 4. Isoproterenol caused a decrease in the volume of gastric juice and acid secretion, however, the ulcerogenesis was similar to that of the control. 5. Gastric function as well as ulcerogenesis was little affected by a high dose of clonidine. From the above results, it is suggested that central adrenergic activation inhibits cold-restraint induced ulcerogenesis via adrenergic alpha and dopaminergic receptors, and that this effect may be mediated by a decrease in gastric acid secretion. It is also suggested that other factors may be involved in this antiulcerogenic effect.

• Journal of Food Hygiene and Safety
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• v.13 no.3
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• pp.252-257
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• 1998

Bamboo salt has been used as a traditional remedy for gastric ulcer and gastro-intestinal disorders. It is produced by baking the salt packed in bamboo cylinder nine times under the fire of pine tree. Three of commercially available bamboo salt products (bamboo salt A, B, and C) were characterized by qualitative and quantitative analyses using inductively coupled plasma (ICP) spectrometer, ion chromatograph (IC), X-ray diffractometer (XRD), and electron microscope (EM). Compared with crude salt, the contents of iron, silicon, potassium, and phosphate in the bamboo salt products were higher whereas the sulfate content was lower. Water-insoluble fraction of bamboo salts contained the following compounds; MgO, $SiO_2,\;Mg_2Si0_4,\;and\;CaMgSi0_4$. The study on the microscopic structures of the bamboo salts were shown to have smooth surface and fused shape compared with crude salt. Among the three bamboo salt products, product A was used to test a possible inhibitory effect on gastric acid secretion. Each test material (bamboo salt A, crude salt, and reagent-grade NaCl) was given orally to Sprague-Dawley rats at doses of 0.2, 1.0, and 2.0 g/kg for 28 days before pyrolus ligation. Twenty four hours after the last administration of the test materials, volume, pH, total acidity, and pepsin activity of gastric juice were measured by the Shay-ligation method. No significant differences were observed in the secretion of gastric acid between treated groups (bamboo salt-, crude salt- and reagent-grade NaCI-treated groups) and control group (distilled water-treated group). This result demonstrated that bamboo salt did not exert anti-ulcer activities in experimental animals used in the present study.

• Journal of Life Science
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• v.14 no.6 s.67
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• pp.925-930
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• 2004

Antioxidant activity and antimutagenic activities with and without simulated gastric digestion of hot water extracts from white and yellow onions were investigated as compared to BHT and ascorbic acid as control Contents of total phenol and flavonoid in hot water extract of yellow onion were higher than those of white one. The scavenging activity of hydrogen peroxide of both extracts were increased in direct proportion to added their concentration. Antioxidant activity and reducing power of the hot water extract were elevated through analysis of $\beta-carotene-linoleate$ system and were lower than those of BHT and ascorbic acid. Antimutagenic activity after simulated gastric digestion of hot water extract of white and yellow onions was observed against mutagen IG and MNNG on Salmonella typhimurium TA80 and TA100. Extract of yellow onion was higher in antimutagenic activity than that of white one. In conclusion, these results suggested that phenol and flavonoid in hot water extract from yellow and white onions may play an important role in the antioxidant and antimutagenic activities.

• CELLMED
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• v.5 no.4
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• pp.28.1-28.6
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• 2015

This current study investigated the anti-ulcer activity of 2 types of virgin coconut oil (VCO-A and VCO-B) and coconut oil (CO). Sprague-Dawley of male rats divided into 6 groups and each group consisted of ten rats. Rats were then treated with either VCO or CO and then were then anaesthetized and pyloric ligation was performed. The anaesthesia was discontinued and the animal usually recovered consciousness within less than an hour. Three hours later, the animal was then again anaesthetized and sacrificed with chloroform. Stomach removed and its content subjected to measurement of volume and pH. The results revealed VCO-B and VCO-A (100%) significantly inhibited (p < 0.001) the volume of gastric juice secreted by the control rats by 66.81% and 51.53%, respectively. Followed by CO 42.80%. While the inhibition of gastric juice for positive control rats which treated with ranitidine (100 mg/kg) was only 22.38%. The total acid output was reduced by the oils to 70.80%, 74.16% and 40.45% for VCO-A, VCO-B and CO respectively compared to control group. Ranitidine reduced the total acid output by 34.83%. In conclusion, prevention of gastric lesions in rats by VCO was found to increase the mucous and decrease the acid volume, total acid contents and ulcer scoring. The treatment of VCO affects the all parameters that influence the initiation and perpetuation of ulceration.

• The Korean Journal of Physiology
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• v.28 no.2
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• pp.143-150
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• 1994

The whole-cell mode of the patch clamp technique was used to study $Ca^{2+}-activated\;Cl^-\;current$ $(I_{Cl_{Ca}})$ in gastric antral myocytes. Extracellular application of caffeine evoked $Ca^{2+}-activated\;current$. In order to isolate the chloride current from background current, all known systems were blocked with specific blockers. The current-voltage relationship of caffeine-induced current showed outward rectification and it reversed at around $E_{Cl^-}$. The shift of reversal potential upon the alteration of external and internal chloride concentrations was well fitted with results which were calculated by the Nernst equation. Extracellular addition of N-phenylanthranilic acid and niflumic acid which are known anion channel blockers abolished the caffeine induced current. Intracellular application of a high concentration of EGTA also abolished this current. Application of c-AMP, c-GMP, heparin, or $AIF^-_4$ made no remarkable changes to this current. Sodium replacement with the impermeable cation N-methylglucamine or with $Cd^{2+}$ rarely affected this current. From the above results it is suggested that the caffeine induced current was a $Cl^-$ current and it was activated by intracellular $Ca^{2+}$.

• Nutritional Sciences
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• v.9 no.3
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• pp.152-158
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• 2006

Helicobacter pylori (H. pylori) infection rapidly stimulated either COX-2 or 5-LOX and released arachidonic acid metabolites that have been considered as pivotal mediators in H. pylori-induced inflammatory responses. To determine whether red ginseng extract (RGE) can suppress the biosynthesis of 5(S)-hydroxyeicosatetraenoic acids (HETE), a precursor metabolite of leukotrienes B4 (LTB4) in H. pylori-provoked inflammatory responses in gastric epithelial cells, the biosynthesis of monohydroxy fatty acids was measured using radioactive arachidonic acid and validated by RP-HPLC using non-radioactive AA as substrate in AGS cells cocultured with H. pylori (ATCC 43504) with or without pretreatment of RGE. Among three known major HETEs, H. pylori infection specifically induced the biosynthesis of $^{14}C-5(S)-HETE$ rather than the complex of $^{14}C-15S-/^{14}C-12(S)-HETE$ from $^{14}C-AA$, concomitantly obtained by HPLC(p<0.01). RGE, 1 to $100{\mu}g/ml$, selectively suppressed H. pylori-stimulated $^{14}C-5(S)-HETE$ production implying the attenuation of 5-lipoxygenase activity, of which was similar to known LOX inhibitor NDGA $(10{\mu}M)$ (p<0.01). However, the amount of 5(S)-HETE was significantly reduced by higher dose of RGE $(100{\mu}g/ml)$ (p<0.05). These results indicated that LOX pathway might be one of principle pathogenic mechanisms of H. pylori and red ginseng could be a nutraceutical against H. pylori infection through inhibiting action of LOX activity.

• Korean Journal of Pharmacognosy
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• v.15 no.3
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• pp.128-133
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• 1984

The extracts of Yukgunja-tang which has been used in some of gastroin testinal disorders were examined for secretion of gastric juice and movement of isolated stomach of rabbit. Experiments were performed with the dried extract of Yukgunja-tang (sample I) and the dried extract compound made of each drug of Yukgunja-tang (sample II). The secretion of gastric juice at the doses of 25.0 and 50.0mg/kg p.o. of sample I showed the decreases of 34.3 and 43.3%, respectively, as compared with control group, whereas the secretion at a dose of 76.8g/kg of sample II showed 43.1%. In gastric acid secretion, sample I showed 50.0% decrease at a dose of 50.0mg/kg and sample II showed 46.2% decrease at a dose of 76.8mg/kg. In pepsin output sample I showed 17.8 and 23.4% decreases at a dose of 25.0 and 50.0mg/kg, respectively, whereas sample II showed 22.5% decrease at a dose of 76.8mg/kg. The isolated stomach of rabbit showed dose-responsive contraction by addition of sample I, however the contraction was not observed by sample II.