• 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.

• Journal of Physiology & Pathology in Korean Medicine
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• v.24 no.6
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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.

• Advances in Traditional Medicine
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• v.4 no.4
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• pp.253-260
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• 2004

Zosterin is a pectin from a seagrasses of the family Zosteraceae. Zosterin was given to rats intragastrically once 1h before the emotional stress or injection of indomethacin, or administration of 2, 4-D solution daily for seven days at dose of 100 mg/kg. The data obtained demonstrate that zosterin enhances resistance of the stomach tissue to various ulcerogenic factors (emotional stress, indomethacin, pesticide 2, 4-D). It was shown to possess a gastroprotective effect, which is accompanied by diminution of the number and sizes of destructive regions in the gastric mucosa during the ulcer affection, as well as reduction of ATP and glycogen deficit, decrease of lactate excess, and normalization of the energy balance in the gastric mucosa. According to its antiulcer effect, zosterin may be recommended for application in prevention and treatment of stomach diseases together with the basic therapy.

• Journal of Pharmacopuncture
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• v.17 no.3
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• pp.40-49
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• 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 Sasang Constitutional Medicine
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• v.14 no.1
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• pp.100-111
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• 2002

1. The Purpose of study An experimental study has done to examine the effect of defense on gastric mucosal damage of Jowesungcheong-tang. 2. The Material and Method of study Mice had intragastric injected with JST extract before indome thacin treatment which induces hemorrh age erosion artificially. General morphology, infiltrative cell in mucosa, the distribution of UEA-I, COX-1, MAC-1. ICAM, and Apoptotic cell were objected (Ahhreviation) JST :Jowesungcheong-tang, UEA-I : ulex europaeus agglutinin-I, COX-1: cyclooxyhenase-1, ICAM : intercellular adhesion molecule-1, GPE : Gastropathy elicitated mice 3. The results and Conclusions of study 1) The degree of hemorrhage erosion in GPE-group had increased conspicuously in gastric gland proper. JST -group were the same as normal 2) The noticeable increase of granular lecocytes and lymphocytes in GEP-group were seen, but in JST group, the configuration is decreased 3) The decrease of UEA-I positive reacted cells, COX-1, surface epithelial cells and the increase of MAC-l positive cells, ICAM-l positive cells had shown in GPE-group, but in JST-group UEA-I positive cells, COX-1 surface epithelial cells were in creased and MAC-1 positive cells, ICAM-l positive cells were decreased than GPE-group. 4) A number of apoptotic cells were distributed in hemorrhage erosion. The remarkable decrease of apoptotic cells were shown in JST-group.

• Journal of Yeungnam Medical Science
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• v.9 no.2
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• pp.342-350
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• 1992

To investigate the effect of bile acid on gastric mucosa, we performed biologic test using Sprague-Dawley rat. Mixture solution of TDCA 15mM and HCl of pH 3 was given into stomach to one group and HCl of pH 3 was given into stomach to another group. The significant gastric mucosal change was vasodilatation and edema, that was disappeared progressively. These findings suggest the bile acid can damage gastric mucosa.

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

• Journal of Microbiology and Biotechnology
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• v.26 no.5
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• pp.823-828
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• 2016

The present study investigated the protective effect of naturally purified 4-(3,4-dihydroxyphenyl)-3-buten-2-one (DHP) from Phellinus linteus against naproxen-induced gastric antral ulcers in rats. To verify the protective effect of DHP on naproxen-induced gastric antral ulcers, various doses (1, 5, and 10 μg/kg) of DHP were pretreated for 3 days, and then gastric damage was caused by 80 mg/kg naproxen applied for 3 days. DHP prevented naproxen-induced gastric antral ulcers in a dose-dependent manner. In particular, 10 μg/kg DHP showed the best protective effect against naproxen-induced gastric antral ulcers. Moreover, DHP significantly attenuated the naproxen-induced lipid peroxide level in gastric mucosa and increased the activities of radical scavenging enzymes, such as superoxide dismutase, catalase, and glutathione peroxidase, in a dose-dependent manner. A histological examination clearly demonstrated that the gastric antral ulcer induced by naproxen nearly disappeared after the pretreatment of DHP. These results suggest that DHP can inhibit naproxen-induced gastric antral ulcers through prevention of lipid peroxidation and activation of radical scavenging enzymes.

• The Journal of Internal Korean Medicine
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• v.31 no.3
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• pp.401-414
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• 2010

Objectives : This study was carried out to investigate the effects of Soche-hwan extract on indomethacin-induced gastric mucosal lesions of mice. Methods : Experimental mice were divided randomly into four groups. The normal group, the gastropathy group of gastro-inflammation elicited mice, the misoprostol group of mice administered misoprostol after gastro-inflammation elicitation and the Soche-hwan group of mice administered Soche-hwan after gastro-inflammation elicitation. Results : The hemorrhagic erosion of gastric mucosa, the damage of arrangement of mucous secreted cells and HSP70 increased in the gastro-inflammation elicited group, but decreased significantly in the misoprostol and Soche-hwan extract administered groups. Cell proliferation of gastric mucosa decreased in the gastro-inflammation elicited group, but increased significantly in the misoprostol and Soche-hwan extract administered groups. The distribution of mucosal neck cells and mucosal surface cells and PNA positive reactions of surface mucus cells decreased in the gastro-inflammation elicited group, but increased significantly in the misoprostol and Soche-hwan extract administered groups. COX-1 positive cells decreased in the gastro-inflammation elicited group, but increased significantly in the misoprostol and Soche-hwan extract administered groups. iNOS mRNA and COX-2 mRNA increased in the gastro-inflammation elicited group, but decreased significantly in the Soche-hwan extract administered group. NF-kB p65, iNOS and COX-2 increased in the gastro-inflammation elicited group, but decreased significantly in the misoprostol and Soche-hwan extract administered groups. Conclusion : Soche-hwan extract had excellent effects on indomethacin-induced gastric mucosal lesions in mice.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1998.11a
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• pp.124-124
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• 1998

Portal hypertensive gastropathy (PHG) is part of a complex syndrome which occurs as a complication of chronic liver disease and portal hypertension. The gastric mucosa in these patients shows typical congestion of ‘mosaic-like’ pattern and vulnerable to various noxious agents such as NSAIDs and ethanol. We previously reported that DA-9601, a quality-controlled extract from Artemisia asiatica, exhibits cytoprotection against various gastritis models. In the present study we investigated the effect of DA-9601 on ethanol-induced gastric damage in PHG rats. Experimental PHG was produced by CBD ligation in SD rats. DA-9601 was orally administered at a dose of 30 mg/kg or 100 mg/kg daily for 2 weeks.