• The Korean Journal of Physiology and Pharmacology
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• v.2 no.4
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• pp.511-519
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• 1998

This study investigated the role of nitric oxide on the oxidative damage in gastric mucosa of rats which received ischemia/reperfusion and its relation to mucus. Nitric oxide synthesis modulators such as L-arginine and $N^G-nitro-L-arginine$ methyl ester, and sodium nitroprusside, a nitric oxide donor, were injected intraperitoneally to the rats 30 min prior to ischemia/reperfusion which was induced by clamping the celiac artery and the superior mesenteric artery for 30 min and reperfusion for 1 h. Lipid peroxide production, the contents of glutathione and mucus, and glutathione peroxidase activities of gastric mucosa were determined. Histological observation of gastric mucosa was performed by using hematoxylin-eosin staining and scanning electron microscopy. The result showed that ischemia/reperfusion increased lipid peroxide production and decreased the contents of glutathione and mucus as well as glutathione peroxidase activities of gastric mucosa. Ischemia/reperfusion induced gastric erosion and gross epithelial disruption of gastric mucosa. Pretreatment of L-arginine, a substrate for nitric oxide synthase, and sodium nitroprusside prevented ischemia/reperfusion-induced alterations of gastric mucosa. However, $N^G-nitro-$ L- arginine methyl ester, a nitric oxide synthase inhibitor, deteriorated oxidative damage induced by ischemia/reperfusion. In conclusion, nitric oxide has an antioxidant defensive role on gastric mucosa by maintaining mucus, glutathione, and glutathione peroxidase of gastric mucosa.

• Proceedings of the Korean Nutrition Society Conference
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• 2003.10a
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• pp.71-71
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• 2003

• Journal of Veterinary Clinics
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• v.30 no.1
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• pp.5-11
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• 2013

Acute gastric ulcer is caused by the unbalance between cell proliferation and apoptosis in gastric mucosa. Platycodin D (PD) has been reported to have a variety of pharmacological properties, including antioxidant and antiin-flammatory effect. In the present study, we investigated the protective effect of PD on the basis of cell proliferation/apoptosis and cyclooxygenase-2 (COX-2) expression in the acute gastric ulcer induced by ibuprofen in Rats. Acute gastric damage was induced by the repeated treatment of ibuprofen (200 mg/kg) with 8 hrs interval in a day. PD was orally administrated at concentrations of 2.5 and 5 mg/kg every day for 5 days before the induction of acute gastric ulcer. Macroscopically, ibuprofen caused a significant increase in the number of lesions in the gastric mucosa. But pretreatment of PD significantly reduced ibuprofen-induced gastric lesion score and prevented excessive mucus depletion in gastric mucosa. Also, pretreatment of PD counteracted significantly Ki-67 decrease in the proliferating zone of gastric glandular portion and highly reduced or delayed apoptotic cells on TUNEL assay. In addition, COX-2 expression was increased in gastric mucosa bearing erosions or ulcers but pretreatment of PD reduced COX-2 expression in gastric lesions. These results show that pretreatment of PD has a protective effect against ibuprofen-induced gastric damage, not only by counteracting a decrease of cell proliferation, but also by inhibiting or delaying apoptosis via regulation of COX-2 within the gastric mucosa.

• Journal of Physiology & Pathology in Korean Medicine
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• v.30 no.4
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• pp.257-265
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• 2016

The aim of this study was to investigate the effects of Ulmi Pumilae cortex extracts on acute reflux esophagitis rats induced by pylorus and forestomach ligation operation. 40 rats were divided into five groups; Normal group, Sham group, Control group, T1 group and T2 group. 4 groups has a laparotomy after controled 2weeks and sham group, T1 group, T2 group has ligation in stomach. After laparotomy, all group`s body weight, gastric volume, gastric juice PH, SOD activities, catalase activities, lipid peroxidation, total glutathione, the effects on esophageal and stomach mucosa damage were checked. There was significant statistical differences between control group and Ulmi Pumilae cortex extracts adminitration groups(T1 and T2 group) in terms of gastric volume decreasing. Also, adminitration groups has significant effect than control group in decreasing mucosa damage. SOD(superoxide dismutase) and catalase activities has a significant statistical differences between control group and T2 group not in T1 group. These results suggest that the medication of Ulmi Pumilae cortex extracts is effective for the treatment of acute reflux esophagitis in terms of decerasing gastric volume and mucosa damage. Especially, the results were shown to be more positive in High-dose administration group (T2 group) than in Low-dose administration group (T1 group) in SOD and catalase activities.

• The Korean Journal of Pharmacology
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• v.31 no.3
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• pp.313-321
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• 1995

Conflicting data have been reported on the effect of nicotine on gastric mucosal damage. To elucidate the effect of chronic intermittent nicotine on gastric mucosal damage, intragastric nicotine (5 mg/kg, 10 mg/kg) was administered twice per day for 9 days. Gastric mucosal damage was created by s.c. injection of a large dose (1.2 mg/kg) of pentagastrin followed by pylorus ligation for 6 hours. Nicotine treated rats showed reduced gastric mucosal damage about 50% of the control. To examine the mechanism of the protective effect of nicotine, gastric perfusion experiments were done. Basal acid secretion was not affected by intragastric or intravenous nicotine. However, pentagastrin-stimulated acid secretion markedly inhibited by a bolus injection of nicotine, and this response was dose-related. These data indicates that chronic intermittent administration of nicotine protects gastric mucosa against gastrin-induced gastric mucosal damage, and nicotine-induced inhibition of gastrin-stimulated acid secretion has an important role for the protective effect of nicotine. Considering reports concerning nicotine's aggravating effect on the gastric mucosal damage, it is suggested that the methods of administration of nicotine may be an important decisive factor of the divergent action of nicotine on the gastric mucosa.

• International Journal of Industrial Entomology and Biomaterials
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• v.35 no.1
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• pp.14-21
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• 2017

Gastric ulcer is a clinical symptom characterized by inflammation of the gastric mucosa. Stress and alcohol consumption have been identified as the major cause of gastric ulcer. However, the effects of silkworms on ethanol-induced gastric ulcer have not been studied yet. The mature silkworms that are difficult to eat have become easier to ingest due to recent technological development to make steaming and freeze-drying mature silkworm larval powder (SMSP). In this study, we investigated whether three silkworm varieties, Baekokjam, Golden-silk and Yeonnokjam could alleviate ethanol-induced gastric mucosal damage in vivo. Sprague-Dawley rats pretreated with 3 SMSPs (0.1 or 1 g/kg BW) or normal diet (AIN-76A) were exposed to absolute ethanol (3 g/kg BW, 3 h) by oral gavage. Morphological examination included ulcer index as a measurement of hemorrhages and hematoxylin and eosin staining was performed to analyze the severity of gastric ulcer. Results of macroscopic examination suggested that all 3 SMSPs pretreatment significantly protected gastric mucosa against ethanol-induced damage. Microscopic observations demonstrated significant mucosal erosion and inflammation in ethanol-treated rats, which was abrogated in rats pretreated with 3 SMSPs. In addition, pretreatment with all 3 SMSPs showed significant decreases the expression of pro-inflammatory mediators, IL-6 and cyclooxygenase-2. Among SMSP from 3 varieties of silkworm, preadministration of 1 g/kg Baekokjam SMSP showed the most effective protective effect against ethanol-induced gastric ulcer. These results suggest that Baekokjam SMSP can be a potential gastroprotective agent against ethanol-induced gastric ulcer.

• Journal of Pharmaceutical Investigation
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• v.31 no.1
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• pp.27-35
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• 2001

To evaluate the site-specific permeation of aspalatone (acetylsalicylic acid maltol ester, AM) through gastrointestinal tract, the enzymatic degradation and permeation studies were carried out using gastric, duodenal and jejunal mucosae of rabbits. It was found that $15.2{\pm}11.4%$, $11.6{\pm}5.2$ and $0.8{\pm}0.6%$ of the donor dose of AM, salicylmaltol (SM) and aspirin (ASA) permeated through the upper gastric mucosa after 8 hr of permeation, respectively. After 8 hr of AM permeation, SM and ASA were measured to be $15.0{\pm}1.7$ and $2.6{\pm}0.8%$ of the dose in the donor solutions, respectively, and salicylic acid (SA) was not detected even after 6 hr, suggesting a very low gastric damage. For the gastric mucosa, the increase of donor dose from 100 to $1,000\;{\mu}g/ml$ increased the permeation flux dose-dependently (r=0.9905). For the duodenal and jejunal mucosae, however, AM was fully degraded into SM and SA due to the esterase activities within 30 min. AM and ASA were not detected in the receptor solution. This result indicates that AM is not a prodrug of ASA. Addition of potassium fluoride (0.5%) into the donor solution delayed the degradation of AM, but did not allow the permeation through duodenal mucosa even by the inhibition of esterase activity. The addition of $dimethyl-{\beta}-cyclodextrin$ and $2-hydroxypropyl-{\beta}-cyclodextrin$ (5%) into the donor solutions also did not show favorable effects on the permeation of AM through various mucosae. In comparison of permeation rates of AM and ASA through the upper gastric mucosa, the flux of ASA was 4.2 times faster than AM based on the molar concentration. ASA also was fully degraded in the donor solutions faced with duodenal and jejunal mucosae within 2 hr, and was not detected in the receptor solution, suggesting a slower metabolism compared with AM.

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.05a
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• pp.84-84
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• 2002

Abstract To study the status of oxidative DNA damage in Helicobacter pylori infection in more details, gene-specific oxidative DNA damage was investigated by examining oxidative DNA damage to individual genes. This was done by determining the loss of PCR product of a targeted gene before and after gastric mucosal DNA was treated with 8-hydroxyguanine glycosylase, which cleaves DNA at the 8-hydroxyguanine residues.(omitted)

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2002.05a
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• pp.84-84
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• 2002

• Journal of Ginseng Research
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• v.25 no.4
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• pp.141-149
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• 2001

The effect of ginseng on gastric ulcer and gastric acid secretion was investigated in pylorus-ligated rats. Methods: Sprague-Dawley strain rats were used after 24 hours fast. Pylorus-ligation was performed under light ether anaesthesia, then gastric mucosal damage was evoked in conscious pylorus-ligated rats by the administration of subcutaneous (s.c.) indomethancin (20mg/kg), s.c. histamine (150mg/kg) or by pylorus-ligation (Shay ulcer). Ginseng was given by intragastric (i.g.) or intraperitoneal (i.p.) route simultaneously with the ulcerogens. Rats were killed after 3h (indomethacin) and histamine models) or after 18h (Shay ulcer), when the gastric secretory responses, the number and severity of gastric mucosal lesions and mucosal mucus content deetermined. the effect of i.p. ginseng on basal gastric acid secretion and on gastric acide secretion in indomethacin (20mg/kg, s.c.)-treated rats was also investigated in urethane anesthetized rats. Gastric acid secretion was measured by flushing of the gastric lumen with saline every 15min through an oesophageal cannula. Results: In conscious pylorus-ligated rats, i.g. ginseng(12.5-50mg/$m\ell$; 50-200mg/kg) protected against gastric mucosal lesions evoked by s.c. indomethacin or s.c. histanmine in the d3-h pylorus-lighted rat, withoutmodifying gastric acid secretory responses. Ginseng given i.p. (150 or 200mg/kg) did not reduce the gastric lesions produced by histamine or by ligating the pylorus (Shay ulcer) Ginseng given orally in 50mg/$m\ell$ (200mg/kg) increased gastric mucus secretion in saline- and indomethacin-treated conscious pylorus-ligated rats. In anaesthetized rats ginseng (50 or 200mg/kg) did not modify basal gastric acid secretion or gastric acid secretion in the indomethacin-treated rats. Conclusions: ginseng given orally exerts gastroprotective effects in the rat stomach. Such anti-ulcer effect does not involve changes in gastric acid secretory responses. In addition, ginseng possesses stimulatory effect on gastric mucus secretion, which could be one mechanism by which the compound exerts its antiulcer effect. Our data are in favor for a beneficial effect for topically applied ginseng on the gastric mucosa.