• Journal of Gastric Cancer
• /
• v.1 no.1
• /
• pp.4-9
• /
• 2001

Purpose: The trefoil factor family 1 (TFF1) has a protective effect against gastric mucosal damage induced by nonsteroidal anti-inflammatory drugs or ethanol. In addition, a TFF1 knockout mouse model has exhibited circumferential adenomas with high-grade dysplasia, of which $30\%$ progressed into frankly invasive carcinomas. We tried to determine whether the expression pattern of the TFF1 could be involved in the development of sporadic gastric carcinomas. Materials and Methods: We examined TFF1 expression in a series of 43 sporadic gastric carcinomas and 18 gastric adenomas by immunohistochemistry. Results: Strong positive TFF1 staining was identified primarily in the normal gastric mucosa, mainly in the cytoplasm of the superficial and foveolar epithelium. We found TFF1 expression in $55.8\%$ (24 out of 43) of the gastric carcinomas and in $16.7\%$ (3 out of 18) of the gastric adenomas. Statistically, TFF1 immunoreactivity was significantly higher in diffuse-type ($82.4\%$) than in intestinal-type ($38.5\%$) carcinomas(p=0.0058, Fisher's exact test). Conclusion: Our findings provide sufficient evidence that the expression of TFF1 in gastric cancer may simply disclose gastric-type differentiation of neoplastic cells and provide further support for the existence of at least two pathways of malignant transformation of the gastric mucosa: one via intestinal metaplasia and adenomatous dysplasia, leading to glandular carcinomas with intestinal-type differentiation, and the other via hyperplastic changes or de novo changes, leading to diffuse carcinomas and to a subset of glandular carcinomas displaying gastric-type differentiation.

• Journal of Physiology & Pathology in Korean Medicine
• /
• v.24 no.6
• /
• pp.970-975
• /
• 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 Pharmacopuncture
• /
• v.17 no.3
• /
• pp.40-49
• /
• 2014

Objectives: The gastric ulcer is a common disorder of the stomach and duodenum. The basic physiopathology of a gastric ulcer results from an imbalance between some endogenous aggressive and cytoprotective factors. This study examined whether Ganoderma lucidum pharmacopuncture (GLP) would provide protection against acute gastric ulcers in rats. Methods: Sprague-Dawley rats were divided randomly into 4 groups of 8 rats each: normal, control, normal saline (NP) and GLP groups. The experimental acute gastric ulcer was induced by using an EtOH/HCl solution and the normal group received the same amount of normal saline instead of ethanol. The NP and the GLP groups were treated once with injections of saline and GLP, respectively. Two local acupoints were used: CV12 (中脘) which is the alarm point of the Stomach Meridian, and ST36 (足三里), which is the sea point of the Stomach Meridian. The stomachs from the rats in each group were collected and analyzed for gross appearance and histology. Also, immunohistochemistry staining for BAX, Bcl-2 and TGF-${\beta}1$ was performed. Results: Histological observations of the gastric lesions in the control group showed comparatively extensive damage of the gastric mucosa and necrotic lesions had penetrated deeply into the mucosa. The lesions were long, hemorrhagic, and confined to the glandular portions. The lesions were measured microscopically by using the clear depth of penetration into the gastric mucosal surface. The length and the width of the ulcer were measured and the inhibition percentage was calculated. Wound healing of the acute gastric ulcer was promoted by using GLP, and significant alterations of indices in gastric mucosa were observed. Such protection was shown by gross appearance, histology and immunohistochemistry staining for BAX, Bcl-2 and TGF-${\beta}1$. Conclusion: These results suggest that GLP administered at CV12 and ST36 can provide significant protection to the gastric mucosa against an ethanol-induced acute gastric ulcer.

• Journal of Food Hygiene and Safety
• /
• v.31 no.4
• /
• pp.286-293
• /
• 2016

This study is an experiment for gastric protective effects of ursolic acid. In order to identify the effects of ursolic acid on gastrointestinal disorder, acute and chronic gastritis were also observed using HCl ethanol and indomethacin-induced gastric lesion models, respectively. As for gastric acid, it was also identified through proton pump ($H^+/K^+-ATPase$) inhibiting activity. In regards to protective factor for gastric damage, prostaglandin $E_2$ ($PGE_2$) was quantitatively analyzed. Antibacterial activity experiment was done on Helicobacter pylori (H.pylori), which is known to be the causing factor of chronic gastritis, gastric ulcer and gastric cancer. By making use of AGS cell, it was confirmed that ursolic acid was involved in apoptosis of gastric cancer cell through 4',6-diamidino-2-phenylindol (DAPI) staining and flow cytometry analysis. As a result, ursolic acid reduced gastric lesions caused by HCl ethanol and indomethacin. Ursolic acid inhibited acid secretion by inhibiting proton pump ($H^+/K^+-ATPase$), which is the gastric acid secreting enzyme involved at the final phase of gastric acid secretion. And ursolic acid was identified with gastric mucosa protection effects by increasing the concentration of $PGE_2$, a protective factor of gastric mucosa preservation. The antibacterial activity on H. pylori, which is aggressive factor in gastrointestinal disorder, ursolic acid showed inhibitory effects on H. pylori colonization. In the DAPI nuclear staining, unlike the control group, shape of the nucleus has deformed, and has been observed either shrinked cell or chromatin condensation phenomenon. In the Flow cytometry assay, confirmed the growth rate of apoptosis in a concentration-dependent manner.

• Korean Journal of Fisheries and Aquatic Sciences
• /
• v.47 no.6
• /
• pp.765-769
• /
• 2014

We examined the protective effects of Pyropia yezoensis glycoprotein (PYGP) against ethanol-induced gastric damage. The experimental animals were divided into four groups. They were treated with distilled water (control), ethanol alone (EtOH), ethanol + PYGP 150 mg/kg BW (EtOH+150), or ethanol + PYGP 300 mg/kg BW (EtOH+300). The groups were treated for 4 weeks. We measured mitogen-activated protein kinase (MAPK), the apoptotic signaling pathway, and PARP activity in gastric tissues obtained from the rats. Ethanol consumption increased apoptotic signal activity and ERK, JNK, and p38 phosphorylation. PYGP reduced the apoptotic signaling pathway activity and ERK, JNK, and p38 phosphorylation. Furthermore, PYGP regulated Bcl-2 family expression. In light of these findings, PYGP appears to prevent ethanol-induced gastric injury and oxidative stress.

• The Korea Journal of Herbology
• /
• v.24 no.1
• /
• pp.35-40
• /
• 2009

Objectives : The purpose of this study is to evaluate whether or not a pretreatment with Portulaca oleracea has an antioxidant effect in HCl-ethanol induced gastric mucosal damage. Methods : We elucidated the level of reactive oxygen species (ROS), lipid peroxidation, and two important constituents of antioxidant defense such as superoxide dismutase (SOD), glutathione (GSH) in these effects. Results : The oral administration of crude extract from P. oleracea attenuated the gastritic lesion area, submucosal edema and hemorrhage, and mucosal necrosis induced by HCl-ethanol. The MDA levels of control group were higher than those in the rats given the P. oleracea pretreatment. While the GSH levels of control were decreased, the GSH activity on the gastric mucosal layer maintain normal level in rats given the Portulaca oleracea pretreatment before HCl-ethanol induced gastritis significantly increased. However, the SOD activites were not altered by P. oleracea. Conclusions : The administration of Portulaca oleracea have a protective antioxidant effect against the gastric lesion induced by HCl-ethanol and may therefore be a promising drug for gastritis and gastric ulcer.

• Korean Journal of Clinical Laboratory Science
• /
• v.55 no.4
• /
• pp.291-297
• /
• 2023

Gastritis is an inflammation of the gastric mucosa and gastric ulcers are a break in the mucosa of the stomach lining. Past research on gastritis and gastric ulcers has been mainly conducted from the perspective that environmental factors are the primary cause of these gastric diseases. However, recently the importance of genetic factors has been emphasized due to current developments in genetic research. The SLC25A26 gene is believed to be associated with the accumulation of reactive oxygen species. Oxidative stress promotes an inflammatory response, which increases the production of free radicals and causes cellular damage, and these lead to the development of gastric diseases. In this study, the correlation between SLC25A26 and gastric diseases was analyzed. Polymorphisms in SLC25A26 were analyzed in 1,369 domestic gastric disease patients and 7,471 healthy controls. As a result, 11 single nucleotide polymorphisms (SNPs) (in the genotype) and 13 SNPs (in the imputation) showed statistical significance (P<0.05), and high relative risk of gastric diseases. Among them, the rs13874 allele of SLC25A26 showed a highly significant association with gastric diseases. In the genotype-based mRNA expression analysis, the minor allele (C) group showed increased mRNA expression and this could increase oxidative stress. In conclusion, SLC25A26 polymorphisms are associated with gastric diseases. These results may provide a basis for new guidelines for gastric disease management in the Korean population.

• Journal of Life Science
• /
• v.33 no.11
• /
• pp.923-935
• /
• 2023

Rubus crataegifolius (RC), Ulmus macrocarpa (UM), and Gardenia jasminoides (GJ) are well-known folk medicines in Asia used to treat various gastrointestinal disturbances. The present study evaluated the gastroprotective effect of LS-RUG-com, a mixture of commercially prepared powders of RC, UM, and GJ with a ratio of 3:1:2(w/w/w) against HCl/ethanol-induced gastritis, indomethacin-induced ulcers, and esophageal reflux-induced esophageal mucosal damage and Helicobacter pylori infections. In addition, TNF-α and IL-1β expressions were also determined and measured in esophageal tissue. As to HCl/ethanol-induced gastritis, the LS-RUG-com treatment at a dose of 150 mg/kg showed a remarkable anti-gastritis effect. Regarding indomethacin-induced gastric ulcers, the LS-RUG-com treatment had a significant anti-gastric ulcer effect. Furthermore, in the gastroesophageal reflux disease (GERD) model experiment, the LS-RUG-com treatment resulted in the histological recovery of stomach damage and mucosal injuries. Furthermore, the LS-RUG-com treatment led to an increase in gastric content pH, an increase in mucus protection, and a decrease in gastric pepsin output with a significant decrease in TNF-α and IL-1β. As to the Helicobacter pylori infected animal model, LS-RUG-com had a notable inhibitory effect on Helicobacter growth. The use of RC, UM, or GJ in isolation or the LS-RUG-com treatment as whole had good effects in terms of anti-oxidation, anti-neutralization, gastric acid secretion inhibition, and anti-lipid peroxidation, which supported the use of natural products as systemic gastric protective agents. Our results suggest that the LS-RUG-com might be a significant systemic gastroprotective agent that could be utilized for the treatment and/or protection from gastric disturbances and related damage.

• Journal of Korean Medicine Rehabilitation
• /
• v.30 no.3
• /
• pp.57-69
• /
• 2020

Objectives The aim of this study was to investigate the inhibitory effect of ChondroT in indomethacin-induced gastric mucosal injury rat model. Methods Sprague-Dawley rats were randomly assigned to intact, control Joins, Celebrex, ChondroT50 and ChondroT200. Indomethacin (25 mg/kg) was used to induce damage to the gastric mucosal injury. ChondroT was administered by orally to inhibit the indomethacin-induced gastric mucosal injury. At the end of the experiment, pH level in stomach, stomach contents volume, tumor necrosis factor-α (TNF-α) level, interleukin-1β (IL-1β) level, prostaglandin E2 (PGE2) level, myeloperoxidase (MPO) activity, erythrocytes, and thrombocytes were measured. Ophthalmologic and histopathological examination was also analyzed. Results pH level in stomach and Stomach contents volume had no difference between Control, PC-Joins, PC-Cele, ChondroT50 and ChondroT200 group. TNF-α level was decreased in PC-Joins, PC-Cele, ChondroT50 and ChondroT200 group and there were no significant difference. IL-1β level was decreased in PC-Joins group and ChondroT200 group compared to control group. PGE2 level had no significant difference between Control, PC-Joins, PC-Cele, ChondroT50 and ChondroT200 group. MPO level and complete blood count level were decreased in PC-Joins, PC-Cele, ChondroT50 and ChondroT200. Symptom score of ophthalmologic examination was decreased in ChondroT50 and ChondroT200 group compared to control group. Conclusion Based on these results, It could be suggested that ChondroT was effective in reducing damage to the gastric mucosal injury. And further study is needed to conduct a rigorous clinical research.

• The Korea Journal of Herbology
• /
• v.27 no.1
• /
• pp.51-58
• /
• 2012

Objectives : This study was performed to investigate effect of evodiae fructus on acute reflux esophigitis rat induced by pylorus and forestomach ligation operation. Methods : Twenty-four laboratory rats were divided four groups and each group had six rats ; normal intact group, acute reflux esophagitis (RE) control group, two experiment RE group treated extract of evodiae fructus 600 mg/kg (EEF600) and 300 mg/kg (EEF300). All rats was fasted for 18 hr but free water, we induced RE by pylorus and forestomach ligation operation. Intact group and RE control group rats were orally administered a distilled water and two experiment groups were orally administed with EEF 600 mg/5ml/kg and 300 mg/5ml/kg. One hour after, rats were anesthetized, intact group was cut the abdomen open and sutured with 2.0 silk thread. RE control group and EEF group were cut the abdomen open, ligated pyloric canal and forestomach with 2.0 silk thread and sutured. Six hour after the operation, rats were sacrified, collected bloods in the abdominal vein, disectted a esophagus and stomach. The stomach was washed a 1 ml PBS and the esophagus was cut longitudinally and pictured a innter mucosa area to research damages in esophagus. Results : The esophagic tissue damage percentage of reflux esophagitis rat was increased compared to that of normal intact group. But esophagic damage percentage of EEF 600 were significantly decreased compared to that of RE control group. But there was no difference on gastric juice pH between control RE, alpha-tocopherol administration rat group and EEF administration rat group. In esophagus of RE control rat, gastric damage occurred severely and injury percentage of mucosa were increased, but EEF 600 mucous inflammatory damage percentage was significantly compared to that of RE control group. Proinflammatory cytokines such as TNF-alpha, IL-1beta and IL-6 in serum on RE control group were markedly grew than those of intact rat, those of vechicle group treated with EEF 600 and EEF 300 were remarkably decreased compared to production of proinflammatory cytokine of RE control group. In microscopic observation, intact group rat had no hyperemia, mucous injury and exclusion, ulcer and edema. But it could showed mucosa damages, submucosa edema and ulcer in RE control. However, administration of EEF 600 and EEF 300 made esophagus have less inflammation and injury by gastric acid. Conclusions : The results suggest that antiinflammatory Effect of EEF could attenuate the severity of reflux esophagitis and prevent the esophageal mucosal damage, and validate its therapeutic use in esophageal reflux disease.