• Toxicological Research
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• 제30권1호
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• pp.45-48
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• 2014

Helicobacter pylori (H. pylori) is the most important factor of gastric disease in clinical practice. Moreover, smoking, stress and a poor diet may be additive factors for gastric damage. With these factors, increasing infection of H. pylori triggers gastritis, gastric ulcers and gastric cancer. To develop a new protective agent, we are concerned with plant-derived extract. The extract of Coptis chinensis (C. chinensis) and its constituents were investigated to assess their protective activities against gastric damage. The C. chinensis extract showed a scavenging effect against 2, 2-diphenyl-1-picrylhydrazyl (DPPH) and superoxide radicals, inhibition of H. pylori colonization and antiulcerogenic activities in rat. In particular, palmatine derived from C. chinensis was found to be the novel protective agent. It is better than the C. chinensis extract, berberine, a well-known constituent of C. chinensis. We suggest that palmatine from the root cortex of C. chinensis may be a good candidate for the development of new pharmaceuticals to prevent gastric disease.

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

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

• 대한약리학회지
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• 제31권3호
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• pp.313-321
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• 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.

• Journal of Ginseng Research
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• 제44권1호
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• pp.79-85
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• 2020

Background: Helicobacter pylori increases reactive oxygen species (ROS) and induces oxidative DNA damage and apoptosis in gastric epithelial cells. DNA damage activates DNA damage response (DDR) which includes ataxia-telangiectasia-mutated (ATM) activation. ATM increases alternative reading frame (ARF) but decreases mouse double minute 2 (Mdm2). Because p53 interacts with Mdm2, H. pylori-induced loss of Mdm2 stabilizes p53 and induces apoptosis. Previous study showed that Korean Red Ginseng extract (KRG) reduces ROS and prevents cell death in H. pylori-infected gastric epithelial cells. Methods: We determined whether KRG inhibits apoptosis by suppressing DDRs and apoptotic indices in H. pylori-infected gastric epithelial AGS cells. The infected cells were treated with or without KRG or an ATM kinase inhibitor KU-55933. ROS levels, apoptotic indices (cell death, DNA fragmentation, Bax/Bcl-2 ratio, caspase-3 activity) and DDRs (activation and levels of ATM, checkpoint kinase 2, Mdm2, ARF, and p53) were determined. Results: H. pylori induced apoptosis by increasing apoptotic indices and ROS levels. H. pylori activated DDRs (increased p-ATM, p-checkpoint kinase 2, ARF, p-p53, and p53, but decreased Mdm2) in gastric epithelial cells. KRG reduced ROS and inhibited increase in apoptotic indices and DDRs in H. pylori-infected gastric epithelial cells. KU-55933 suppressed DDRs and apoptosis in H. pylori-infected gastric epithelial cells, similar to KRG. Conclusion: KRG suppressed ATM-mediated DDRs and apoptosis by reducing ROS in H. pylori-infected gastric epithelial cells. Supplementation with KRG may prevent the oxidative stress-mediated gastric impairment associated with H. pylori infection.

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

• 대한기관식도과학회지
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• 제1권1호
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• pp.55-63
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• 1995

Gastroesophageal reflux is thought to be an important etiology of the various upper aerodigestive tract disease. To investigate the role of gastric acid and pepsin as an etiologic factor of laryngotracheal stenosis, and the difference of injury by synthetic gastric juice between in ciliated respiratory epithelium and in squamous epithelium, experimental study was carried out using rabbits. Mucociliary transport affected by synthetic gastric juice was also studied in dogs. Synthetic gastric juice of low pH caused serious damage and Impairment of mucociliary transport in the epithelium of the larynx and trachea. Gastric acid played major role in the mucosal damage. Squamous epithelium of vocal folds and pharynx was more resistant to synthetic gastric juice than respiratory epitheium. In conclusion, gastroesophageal reflux may be an etiologic factor in the developement of laryngotracheal stenosis, so the adequate management is necessory In patients of laryngotracheal stenosis.

• The Korean Journal of Physiology and Pharmacology
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• 제2권4호
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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.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2002년도 Current Trends in Toxicological Sciences
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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)

• Archives of Pharmacal Research
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• 제22권1호
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• pp.44-47
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• 1999

Three 1,2-benzothiazine derivatives were synthesized, and their analgesic / anti-inflammatory efficacy and their effect s of gastric irritation were evaluated. Among the three compounds, 39 exhibited the most potent anlagesic action, but the effect was weaker than that of piroxicam. Nonetheless, the compound showed 4 times more potent analgesic action with less gastric damage than did ibuprofen. These compounds did not show anti-inflammatory effect at an oral dose of 5 mg/kg.