• Asian Pacific Journal of Cancer Prevention
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• 제17권4호
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• pp.2099-2103
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• 2016

Background: The gold standard diagnosis of H. pylori related gastritis is evidence of bacteria on histopathological examination of gastric mucosa. Our aim was to study the correlation between gastric mucosal morphology and histopathological severity of H. pylori related gastritis. Materials and Methods: Division was made on morphological features into:Type 1, showing regular arrangement of red dots; Type 2, showing cleft-like appearance; Type 3, with a mosaic appearance; and Type 4, having a mosaic appearance with focal or diffuse hyperemia. Results: Types 1 and 2 gastric mucosal morphologies were statistically significant in predicting an H. pylori negative status (137/145, p<0.01), while Types 3 and 4 were significant a positive status (139/155, p<0.01). The sensitivity, specificity, positive and negative predictive values of Type 3 and 4 morphologies for predicting H. pylori positive were 94.6%, 89.5%, 89.7% and 94.5%, respectively, with a good correlation with inflammation grading (p<0.01). Conclusions: Our study suggests that gastric mucosal morphology can be reliably identified using conventional white light source gastroscopy with good correlation between findings and inflammation grading.

• 동의생리병리학회지
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• 제24권6호
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• pp.970-975
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• 2010

Because Lonicerae Flos has effects of antiinflammatory and antioxidant, we studied an effect of Lonicerae Flos on reflux esophagitis (RE) through those effects. Rats were treated with three different dosages of LF (500, 250 and 125 mg/kg) orally for 14 days before pylorus and forestomach ligation. Six hrs after pylorus and forestomach ligation, we dissected a stomach and examined a stomach volume, gastric acid output, pepsin release in the stomach, total hexose, sialic acid in stomach tissue and histamine contents of sera. The results were compared with an ${\alpha}$-tocopherol (once orally, 1hr before operation, 30 mg/kg) treated group in which the effects on RE were already confirmed. Lonicerae Flos extract (LE) reduced gastric volumes compared to RE control. This indicate that LE protect a stomach mucosa by depressing of gastric acid release and corresponse with a reducing histamine content of serum. And LE decreasd a volume of pepsin in stomach compraed to RE control, LE increased contents of total hexose and sialic acid based on esophageal and gastric mucus. This indicated that an increased mucus by LE protected inflammation of esophagus mucosa and gastric mucosa induced by gastric acid. So, LE suppressed a gasric acid by decreasing a pepsin release in stomach, suppressed an injury of esophagus inducted by gastric acid with increasing esophageal mucus and a minimum dose of LE to RE was 250 mg/kg. The results suggest that antioxidant effects of LF could attenuate the severity of reflux esophagitis and prevent the esophageal mucosal damage, and validate its therapeutic use in esophageal reflux disease.

• Journal of Gastric Cancer
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• 제12권4호
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• pp.254-257
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• 2012

Gastric tuberculosis is rare even in the endemic areas of tuberculosis, and can mimic neoplasm by causing elevation of the mucosa with or without ulceration. Here, we report a case in which a 54-year-old female patient admitted for resection of early gastric cancer was found to have coexisting histopathologically and bacteriologically confirmed gastric cancer and tuberculosis.

• 대한한방내과학회지
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• 제25권3호
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• pp.497-507
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• 2004

This study was carried out to investigate the effects of Ikwitang extract on indomethacin-induced gastric mucosal lesions in mice. Experimental groups were classified into a non-treated group(NM group), a non-administered group(CON group), the Misoprostol-administered group(MI group) and the Ikwitang-extract-administered group(IW group). This study examined the morphological change, distribution of mast cells, mucous surface cells, acid mucose secreted cells, and apoptic cells, BrdU, COX-1, Hsp70, $NF-{\kappa}B\;p50$, PKC, COX-2 and IL-12B of gastric mucosa. Results : The results of this study were as follows: 1. In the Misoprostol-administered group and the Ikwitang-extract-administered group, the hemorrhagic erosion of gastric mucous and infiltrated mast cells decreased. 2. Mucous surface cells and acid mucose secreted cells abserved in the Misoprostol-administered group and the Ikwitang-extract administered group. 3. The distribution of apoptic cells, Hsp70, $NF-{\kappa}B\;p50$, PKC, COX-2, and IL-12B increased in the Control group, but decreased in the Misoprostol-administered group and Ikwitang-extract-administered group. 4. Cells proliferation of gastric mucosa and the COX-l positive cells decreased in the Control group, but increased in the Misoprostol-administered group and the Ikwitang-extract -administered group. The above results suggest the lkwitang extract had beneficial effects on indomethacin induced gastric mucosal lesions.

• Journal of Ginseng Research
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• 제22권1호
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• pp.22-31
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• 1998

Antiulcer effects of ginseng saponin, acidic polysaccharide and methanol extract of Panax ginseng in the patients and experimental animals were reported. Postulated action mechanisms of ginseng were histamine-Ht receptor blocking and increasing gastric blood flow In the present study, the effect of ginsenosides, the biologically active glycosides of ginseng, on gastric acid secretion was examined using gastric cells isolated from human and rabbit gastric mucosa. Ginseng saponin, ginsenoside $Rb_1$, $Rb_2$, $Rg_1$ and $Rh_2$ were tested in unstimulated as well as stimulated gastric cells. Histamine ($10^4$M) and 3-isobutyl-1-methylxanthine ($10^4$M) were used as secretagogues. To investigate the mechanism of ginsenosides on acid secretion, the levels of cAMP and cGMP were monitored in gastric cells. As a result, high concerltration(1mg/ml) of ginseng saponin showed 73-75% of stimulated acid secretion in control gastric cells. However, ginseng saponin had no effect on unstimulated acid secretion and the levels of cGMP and cAMP in gastric cells. Ginsenoside $Rb_1$, $Rb_2$ and $Rh_2$ significantly inhibited stimulated acid secretion. Gastric cGMP levels were increased by all ginsenosides tested while cAMP levels were increased by all ginsenosides in unstimulated state of gastric cells, but increased by ginsenosides ginsenoside $Rg_1$ and $Rh_2$in stimulated state of gastric cells. The results suggest that inhibition of ginseng saponin on gastric acid secretion represents a complex effect of individual ginsenosides, which produce a range of effect on acid secretion. The inhibition site of ginseng saponin on stimulated acid secretion is postulated as post cAMP levels in acid secretary pathway such as protein phosphorylation or proton pump. Nitric oxide may not be involved in the inhibitory effect of ginseng saponin on stimulated acid secretion.

• Asian Pacific Journal of Cancer Prevention
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• 제16권1호
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• pp.71-76
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• 2015

Magnesium sulfate is widely used as a food additive and as an orally administered medication. The aim of this study was to evaluate the possible cytotoxicity of magnesium sulfate on AGS human gastric adenocarcinoma cells and gastric mucosa in mice. A trypan blue exclusion assay was used to determine the reduction in viability of AGS cells exposed to magnesium sulfate, and then effects on cell proliferation were quantified. The role of magnesium sulfate-mediated pro-inflammatory cytokine production in AGS cells was also investigated. mRNA expression for IL-$1{\beta}$, IL-6, IL-8, and TNF-${\alpha}$ was determined by RT-PCR, and secretion of these cytokines was measured by ELISA. Immunohistochemical evaluation of IL-$1{\beta}$, IL-6, and TNF-${\alpha}$ expression was conducted in mouse gastric mucosa. Addition of 3 to 50 mM magnesium sulfate to AGS cells inhibited both cell proliferation and cell viability in a dose-dependent manner. Magnesium sulfate had little effect on production of IL-$1{\beta}$ or IL-6 but significantly inhibited production of IL-8. The animal model demonstrated that magnesium sulfate induced production of IL-$1{\beta}$, IL-6, and TNF-${\alpha}$. These preliminary data suggest that magnesium sulfate had a direct effect on the stomach and initiates cytotoxicity in moderate concentrations and time periods by inhibiting viability a nd proliferation of AGS cells and by regulating expression and/or release of pro-inflammatory cytokines.

• Journal of Ginseng Research
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• 제43권4호
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• pp.550-561
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• 2019

Background: Gastric ulcer (GU) is a common gastrointestinal disease that can be induced by many factors. Finding an effective treatment method that contains fewer side effects is important. 20 (S)-ginsenoside Rg3 is a kind of protopanaxadiol and has shown superior antiinflammatory and antioxidant effects in many studies, especially cancer studies. In this study, we examined the treatment efficacy of 20 (S)-ginsenoside Rg3 on GU. Methods: Three kinds of GU models, including an alcohol GU model, a pylorus-ligated GU model, and an acetic acid GU model, were used. Mouse endothelin-1 (ET-1) and nitric oxide (NO) levels in blood and epidermal growth factor (EGF), superoxide dismutase, and NO levels in gastric mucosa were evaluated. Hematoxylin and eosin staining of gastric mucosa and immunohistochemical staining of ET-1, inducible nitric oxide synthase (NOS2), and epidermal growth factor receptors were studied. Ulcer index (UI) scores and UI ratios were also analyzed to demonstrate the GU conditions in different groups. Furthermore, Glide XP from $Schr{\ddot{o}}dinger$ was used for molecular docking to clarify the interactions between 20 (S)-ginsenoside Rg3 and EGF and NOS2. Results: 20 (S)-ginsenoside Rg3 significantly decreased the UI scores and UI ratios in all the three GU models, and it demonstrated antiulcer effects by decreasing the ET-1 and NOS2 levels and increasing the NO, superoxide dismutase, EGF, and epidermal growth factor receptor levels. In addition, high-dose 20 (S)-ginsenoside Rg3 showed satisfactory gastric mucosa protection effects. Conclusion: 20 (S)-ginsenoside Rg3 can inhibit the formation of GU and may be a potential therapeutic agent for GU.

• 대한한방내과학회지
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• 제37권4호
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• pp.669-677
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• 2016

Reflux esophagitis is a common disease in developed nations. We describe the case of a female patient with endoscopic reflux esophagitis complicated by gastric dysmotility. Both electrogastrography and enterotachography were performed to detect gastric myoelectrical activity and pyloric sphincter function and evaluate gastric motility. The patient was treated only with herbal medications and general acupuncture, with electrical stimulation of the ST.36 (Zusanli) point, in addition to moxibustion therapy. After each primary and secondary treatment, the therapeutic effect was immediately evaluated. At the final follow-up 5 mon after the end of the secondary treatment, the patient’s general condition was assessed, in addition to the mucosa of the esophagus. At follow up, all the patients’ symptoms had disappeared, and the mucosa of the esophagus had returned to normal. We attributed these therapeutic effects to improved gastric dysmotility. To confirm the usefulness of this treatment method, studies of larger numbers of patients with reflux esophagitis treated with Korean traditional medicine are needed.

• Preventive Nutrition and Food Science
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• 제18권2호
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• pp.104-110
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• 2013

Presence of Helicobacter pylori is associated with an increased risk of developing upper gastrointestinal tract diseases. Antibiotic therapy and a combination of two or three drugs have been widely used to eradicate H. pylori infections. Due to antibiotic resistant drugs, new drug resources are needed such as plants which contain antibacterial compounds. The aim of this study was to investigate the ability of GutGard$^{TM}$ to inhibit H. pylori growth both in Mongolian gerbils and C57BL/6 mouse models. Male Mongolian gerbils were infected with the bacteria by intragastric inoculation ($2{\times}10^9$ CFU/gerbil) 3 times over 5 days and then orally treated once daily 6 times/week for 8 weeks with 15, 30 and 60 mg/kg GutGard$^{TM}$. After the final administration, biopsy samples of the gastric mucosa were assayed for bacterial identification via urease, catalase and ELISA assays as well as immunohistochemistry (IHC). In the Mongolian gerbil model, IHC and ELISA assays revealed that GutGard$^{TM}$ inhibited H. pylori colonization in gastric mucosa in a dose dependent manner. The anti-H. pylori effects of GutGard$^{TM}$ in H. pylori-infected C57BL/6 mice were also examined. We found that treatment with 25 mg/kg GutGard$^{TM}$ significantly reduced H. pylori colonization in mice gastric mucosa. Our results suggest that GutGard$^{TM}$ may be useful as an agent to prevent H. pylori infection.

• 대한한방내과학회지
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• 제19권2호
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• pp.185-207
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• 1998

In order to study the immunohistochemical effects of Opae-san on gastric ulcer induced by HCl-aspirin in rats, experiments were done by oral administration and measure histological features of ulcer lesion, scaning electron microscopic appearance, the changes of numbers of parietal cells, chief cells, gastrin and somatostatin-immunoreactive cells. The obtained results are as follows: 1. Ulcerative lesions were numerously detected in control groups especially in junction of cardiac-fundic gastric mucosa and histologically very severe injury to gastric epithelium were observed too but in the Opae-san administrated groups, no gross lesion of ulcer were detected and histologically minor injury of gastric mucosa were observed. Most slight injuries to gastric mucosa were observed in 5 days after treatment. 2. The numbers of parietal cells were remarkably increased in control group but in Opae-san administrated groups appeared significant decrease compared to control groups. Most remarkably decrease of the numbers of parietal cells compared to control groups were observed in 5 days after treatment. 3. The numbers of chief cells were remarkably decreased in control group but in Opae-san administrated groups appeared significant increase compared to control groups. Most remarkably increase of the numbers of chief cells compared to control groups were observed in 5 days after treatment. 4. The numbers of gastrin-immunoreactive cells were remarkably decreased in control group but in Opae-san administrated groups appeared significant increase compared to control groups. Most remarkably decrease of the numbers of gastrin-immunoreactive cells compared to control groups were observed in 5 days after treatment. 5. The numbers of somatostatin-immunoreactive cells were remarkably decreased in control group but in Opae-san administrated groups appeared significant increase compared to control groups. Most remarkably decrease of the numbers of somatostatin-immunoreactive cells compared to control groups were observed in 5 days after treatment. 6. Scaning electron microscopically, severe denude and degeneration of gastric mucosa were observed in control groups but in Opae-san administrated groups the lesions were remarkably decreased compared to control groups.