• 한국영양학회:학술대회논문집
• /
• 한국영양학회 2003년도 추계학술대회 및 정기총회
• /
• pp.71-71
• /
• 2003

• Preventive Nutrition and Food Science
• /
• 제5권1호
• /
• pp.37-41
• /
• 2000

The protective effects of the ethylacetate fraction of persimmon leaves(PEF) against experimentally induced gastric mucosal damage and gastric ulcers were evaluated in ratss. In prophylatic study, 100 mg/kg ethylacetate fraction of persimmon leaves (PEFH) exhibited a total protection of 73.8% and 65.7% against HCl-ethanol and 0.2N NaOH-induced gastric mucosal membrane lesions, respectively, which was superior to cimetidine 50 mg/kg, a commonly used anti-ulcer drug. PEFH showed excellent anti-ulcer effects against pylorus ligation induced gastric ulcers, compared to the control group, however, 50 mg/kg ethylacetate fraction of persimmon leaves (PEFL) and PEFH did not affect ulcers induced by water immersion stress, and that is inferior to cimetidine 50 mg/kg. In conclusion, the results suggest that the ethylacetate fraction of persimmon leaves can be used both in prevention and treatment of experimentally induced gastric mucosal damage and ulcers.

• Advances in Traditional Medicine
• /
• 제6권1호
• /
• pp.53-57
• /
• 2006

The plant Indigofera aspalathoides is used by a large number of tribes in India for the treatment of various hepatic disorders and abscesses. The methanol extract of Indigofera aspalathoides (MEIA) was evaluated for its protective effects on gastric mucosal lesion in Wister albino rats against indomethacin, histamine and ethanol induced gastric mucosal damage. The response to MEIA was assessed using the ulcer index, thiobarbituric acid reactive substance (TBARS), and glutahione level. MEIA pretreatment showed protection against chemical induced gastric mucosal damage, a significant reduction in the ulcer index and TBARS activity and increase glutathione level as compared with that of standard drugs.

• 대한약리학회지
• /
• 제31권3호
• /
• pp.313-321
• /
• 1995

위점막 손상에 미치는 영향에 관한 nicotine의 효과는 아직 정설이 없는 형편이다. 본 연구에서는 nicotine이 위점막 손상에 미치는 영향을 보기 위하여 nicotine (5 mg/kg, 10mg/kg)을 9일간 하루에 두번씩 위내 투여하였다. 위점막 손상은 gastrin (1.2 mg/kg)을 피하 주사함과 동시에 유문부결찰을 6시간 동안 시행하므로 야기시켰다. 그 결과 nicotine 투여군에서 현저한 위점막 손상의 감소를 보였다 (대조군의 50%). 이러한 nicotine의 위점막 보호 효과에 대한 기전을 추구하기 위하여 위관류 실험을 시행하였다. Nicotine은 기초 위산 분비에는 영향이 없었으나 gastrin으로 자극된 위산 분비를 현저히 감소시켰고, 이러한 반응은 nicotine 용량에 비례하였다. 이상의 결과로 보아 nicotine의 장기간 간헐적 투여는 gastrin 투여로 인한 위점막 손상에 보호 효과가 있으며, 이러한 효과는 gastrin으로 자극된 위산 분비를 억압하는 nicotine의 효과가 관련될 것으로 생각된다. 또한 nicotine의 위점막 손상 악화 효과를 관찰한 보고들을 고려하면 nicotine의 위점막 손상에 관한 효과는 nicotine의 투여 방법에 따라 전혀 다르게 나타날 수 있을 것으로 생각된다.

• 대한약학회:학술대회논문집
• /
• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
• /
• pp.129.1-129.1
• /
• 2003

Alcohol, Helicobacter pylori, stress and NSAIDs-activated neutrophils all produce reactive oxygen species (ROS), which play an important role in gastric mucosal damage. Eupatilin is an active component of Artemisia asiatica possessing cytoprotective effect. The effect of eupatilin on the production of ROS and cellular damage in AGS and ECV304 cells were evaluated to prove the cytoprotective action against the above mentioned gastric mucosal cell damages. (omitted)

• Journal of Microbiology and Biotechnology
• /
• 제14권5호
• /
• pp.996-1003
• /
• 2004

Nonsteroidal anti-inflammatory drugs such as indomethacin induce severe gastric mucosal damage in humans and rodents. In the present study, the in vivo protective effect of astaxanthin on indomethacin-induced gastric lesions in rats was investigated. The test groups were injected with indomethacin (25 mg/kg) after the oral administration of astaxanthin (25 mg/kg) for 1, 2, and 3 days, while the control group was treated only with indomethacin. Thiobarbituric acid reactive substances in the gastric mucosa, as an index of lipid peroxidation, increased significantly after indomethacin administration and this increase was inhibited by oral administration of astaxanthin. In addition, pretreatment with astaxanthin resulted in a significant increase of the activities of superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH-px). Histologic examination clearly revealed acute gastric mucosal lesions induced by indomethacin in the stomach of the control group, but were not observed in that of the test group. These results indicate that astaxanthin activates SOD, catalase, and GSH-px, and removes the lipid peroxides and free radicals induced by indomethacin. It is evident that astaxanthin acts as a free radical quencher and antioxidant, and is an effective molecule in the remedy of gastric mucosal lesions.

• 사상체질의학회지
• /
• 제14권1호
• /
• pp.100-111
• /
• 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.

• Biomolecules & Therapeutics
• /
• 제5권2호
• /
• pp.202-210
• /
• 1997

Protective effect of DA-9601, an extract of Artemisia Herb, against ethanol-induced gastric mucosal injury was evaluated in rats. In the prophylactic study, DA-9601 exhibited total protection (99.4%) against absolute ethanol-induced gastropathy, And the protective effect of DA-9601 lasted up to 2 hours, which was longer than those of other contemporary mucoprotectants. In the treatment study, DA-9601 significantly facilitated the healing of 70% ethanol-induced mucosal damage, which was superior to cetraxate, a commonly used anti-ulcer drug. The mechanisms of mucoprotection of DA-9601 were also assessed. DA-9601 increased the release of prostaglandin E$_2$ from murine neutrophils in a dose-dependent manner in vitro. The cytoprotective effect of DA-9601 against ethanol-induced mucosal damage was significantly diminished by the concommitant injection of N$\omega$-nitro-L-arginine methyl ester (L-NAME, 5 mg/kg, i.v.), a non-specific nitric oxide (NO) synthase inhibitor, while it was not affected by preinjection of indomethacin (5 mg/kg, s.c.), a prostaglandins-depletor. And it was found that DA-9601 significantly enhanced adaptive cytoprotective action of 10% ethanol against absolute ethanol (56.9$\pm$6.5 vs 23.0$\pm$3.3 mm$^2$, p<0.05, mean$\pm$SEM), though its exact underlying mechanism remains to be clarified. The present fin[lings demonstrate that DA-9601 exerts gastroprotecticv actions for the stomach against ethanol through several different underlying mechanisms, in which prostanglandins and NO are involved. In conclusion, the results obtained suggest that DA-9601 can be useful both in prevention and treatment of ethanol-induced gastric damage.

• 생약학회지
• /
• 제43권1호
• /
• pp.72-78
• /
• 2012

Alnus japonica Steud (A. japonica) have long been used in the traditional medicine for gastric disorder, hepatitis and fatty liver in Korea. Antiulcer effects of A. japonica hot water extract (AJ ext) were evaluated by in vitro antibacterial activity against H. pylori, by the inhibitory action against the in vitro gastric $H^+/K^+$-ATPase and using rat models of gastric mucosal damage and gastric ulcer induced by HCl-ethanol, indomethacin, and restraint and water-immersion stress. For the determination of antibacterial activity of AJ ext against H. pylori, the activity of urease which released from H. pylori was measured in culture. AJ ext showed weak antibacterial activity against H. pylori with the growth inhibitions of 37% and 61% by adding final concentrations of 500 and $1000{\mu}g/ml$ culture, respectively at 24 h. To observe the inhibitory activity of AJ ext against the $H^+/K^+$-ATPase in hog gastric membrane vesicle, $IC_{50}$ value of AJ ext was $806.3{\mu}g/ml$. Pretreatment of AJ ext (200, 500 mg/kg, p.o.) prevented in a dose-dependent manner the acute gastritis in HCl-ethanol model and the formation of gastric ulcer in indomethacin model and restraint and water-immersion stress model. These results suggest that the AJ ext can be used for prevention and treatment of gastric mucosal damage and ulcers induced by various stress.

• Journal of Ginseng Research
• /
• 제25권4호
• /
• pp.141-149
• /
• 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.