• 생약학회지
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• 제52권4호
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• pp.242-250
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• 2021

Artemisia frigida Willd (AW, Fringed sagewort), which is widespread in Mongolia, is a well-known medicinal plant as a member of the Compositae family. This study aims to explore the gastroprotective effect of water extract of AW on 150 mM HCl/60% ethanol-induced acute gastritis in 5 week old male ICR mice. Total polyphenols, total flavonoid contents, and anti-oxidant activity in vitro in AW were evaluated. First, the gross area of gastric mucosal damage was measured. Then western blot analysis was conducted to determine the possible mechanisms of action underlying the effects of AW. AW administration decreased gastric mucosal damage. Moreover, the group with AW treatment effectively inhibited nicotinamide adenine dinucleotide phosphate (NADPH) oxidase expression associated with oxidative stress. AW treatment enhanced an anti-oxidant effect through the increase of anti-oxidant proteins. Besides, the increased expressions of inflammatory cytokines induced by nuclear factor-kappa B (NF-κB) activation are alleviated through AW treatment. Taken together, AW exerted a gastroprotective effect against gastric mucosal damage. These results indicate that AW could have the potential used as a natural therapeutic drug for the treatment of acute gastritis.

• 생약학회지
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• 제33권3호통권130호
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• pp.252-256
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• 2002

In the previous study, we demonstrated that ginsenoside $Rb_1$ isolated from the butanol fraction of the head of Panax ginseng had significant gastroprotective activity on gastritis and gastric ulcer models in rats. It has been well established that drugs to have capacity of scavenging or inhibiting the generation of reactive oxygen radicals prevent the gastric mucosal injury. Ginsenoside $Rb_1$ was tested on HCl ethanol-induced gastritis in rats, DPPH-induced free radical scavenging effect, MDA assay, GSH activity, and SOD activity in gastric tissue. It showed significant inhibition in HCl ethanol-induced gastritis, and al~o significantly increase of GSH activated SOD. We speculate that the protective effect of ginsenoside $Rb_1$ against HCl ethanol-induced gastric mucosal damage is originated from the increase of GSH and the activation of SOD.

• 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.

• 한국영양학회:학술대회논문집
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• 한국영양학회 2003년도 연합학술대회
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• pp.299.2-299.2
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• 2003

• The Korean Journal of Physiology and Pharmacology
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• 제16권6호
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• pp.399-404
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• 2012

We investigated inhibitory effects of extract containing quercetin-3-O-${\beta}$-D-glucuronopyranoside (ECQ) extracted from Rumex Aquaticus Herba on indomethacin-induced gastric damage in Rats. Gastritis was induced in male Sprague-Dawley rats (200~220 g) by oral administration of indomethacin at a dose of 40 mg/kg. One hour before administration of indomethacin, animals were orally pretreated with ECQ at doses of 0.3, 1, 3 or 10 mg/kg. Six hours after indomethacin administration, the rats were sacrificed and the stomach was excised and opened along the greater curvature, and the surface area of gastric lesion was measured using optical microscope. Superoxide dismutase (SOD), catalase (CAT), myeloperoxidase (MPO) activities and malondialdehyde (MDA) levels were measured by ELISA. Western blot analysis was performed to detect protein expression of SOD-2. Linear hemorrhagic mucosal lesions were observed in the stomach 6 hours after oral administration of indomethacin. Pretreatment with ECQ significantly reduced the severity of the lesions in a dose-dependent manner. It also inhibited the reductions in SOD and CAT activities and SOD expression by the indomethacin-induced gastric damage. In addition, the pretreatment with ECQ significantly suppressed the elevation of the MPO activity and the MDA levels induced by indomethacin. These results suggest that ECQ has the inhibitory effects via antioxidative action against indomethacin-induced gastritis in rats.

• Biomolecules & Therapeutics
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• 제7권4호
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• pp.362-370
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• 1999

Propolis, a natural resinous compound collected from honey bees, contains many biochemical constituents(wax, flavonoids, phenolic compounds, etc.) and has been used in traditional medicines as early as 300 B.C. It was been demonstrated that ethanol, acetylsalicylic acid, ischemia reperfusion, non-steroidal antiin-flammatory drugs and stress induce gastric lesions by promoting the generation of reactive oxygen metabolites. Therefore, some drugs that are capable of scavenging or inhibiting the generation of reactive oxygen radicals might be expected to prevent the gastric mucosal injury. The aim of this study was 1) to examine the antiulcer effect of propolis, 2) to investigate the mechanism of action by determining gastric acid secretion, lipid per-oxidation, mucus content and proton pump ($H^+$/$K^+$-ATPase) activity on gastric mucus in varios experimental models, and finally, 3) to isolate and identify the pure compounds that exert antiulcer activity. Step 2-1 and 2-3 sub-sub fraction shoed a significant reduction of severity of gastirc damage at the dose of 25 mg/kg in various experimental models. We isolated 4 sub-sub-sub fractions by flash column chromatography of Step 2-1 sub-sub fraction and one sub-sub-sub fraction by recrystalization of Step 2-3 sub-sub fraction. The protective effects of propolis sub-sub-sub fraction manifested sifnificant effects in HCl-ethanol induced gastric erosion model and aspirin induced gastric ulcer model. These results showed that the gastric mucosal protective effect of propolis might result from the increase of mucus secretion, free radical scavenging effect as well as the reduction of acid secretion in accordance with the reduction of $H^+$/$K^+$-ATPase activitv. Three compounds were isolated and identified from sub-sub fraction of propolis which showed antiulcer effects. Subsequently, these compounds were identified as a flavonoid, namely, 2-acetoxy-5,7,-dihydroxy-flavanone, galangin and chrysin.

• Journal of Yeungnam Medical Science
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• 제9권2호
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• pp.342-350
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• 1992

십이지장으로 분비되고 위내로 역류될 수 있는 bile acid가 위점막에 끼치는 영향을 알아보기 위해 체중 200-250gm 전후의 Sprague-Dawley 흰쥐를 사용하여 pH 3인 염산과 TCDA 15mM 혼합용액을 위장내에 주입하고 같은 산도의 염산을 위장내로 투여한 대조군과 비교 조사한 결과 다음과 같은 성적을 얻었다. TCDA에 의한 위점막 손상은 TCDA 투여후 75분이 지난 후 제일 저명하게 나타났고 15분, 30분, 120분 및 150분에는 뚜렷한 변화를 관찰할 수 없었다. TDCA 투여후 75분에 나타나는 소견으로는 점막과 점막하조직의 울혈, 혈관 확장, 임파선 확장, 부종 등을 나타내었으며 시간이 경과함에 따라 혈관 확장 및 부종은 점차 소실되는 소견을 나타내었다. 이상의 결과로 보아 TDCA가 급성 위점막 손상을 일으킬 수 있지만 만성적 위점막 손상에 대해서는 여러 조건하에서 더 많은 연구가 있어야 할 것으로 사료된다.

• 대한수의학회지
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• 제46권4호
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• pp.327-335
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• 2006

A stable and reliable Helicobacter pylori (H. pylori) infection animal model would be necessary for evaluating vaccine efficacy and helpful for understanding the pathological mechanism of the organism. The aim of the present study is to investigate the effect of ethanol treatment prior to H. pylori inoculation on associated gastric mucosal injury and to establish ethanol-pretreating animal model to study H. pylori infection. Male Mongolian gerbils were used for the study. H. pylori was orally inoculated after 12 h fasting. 3 h prior to H. pylori inoculation, a group of gerbils was orally treated with absolute ethanol, 60% and 40% ethanol respectively. Another group of animals was treated either with H. pylori culture media alone or with different concentrations of ethanol plus culture media. Gerbils were killed 4 or 8 weeks after H. pylori inoculation. The colonization of H. pylori was confirmed by both histological examination and rapid urease test. Mucosal damage was evaluated grossly and histologically according to the criteria. The colonization of H. pylori and pathological changes in gastric mucosa of the animals were also observed. Although no significant change to the gastric mucose was observed in the animals treated either with H. pylori culture media alone or with different concentrations of ethanol plus culture media, persistent H. pylori infection was seen in the mucosa and mucosal leucocyte infiltration and severe epithelial damage was observed in the Helicobacter and ethanol + Helicobacter groups after 4 weeks. The gross and histological scores were higher in the ethanol + Helicobacter than in the Helicobacter alone group. As the results, ethanol-pretreatment with 60% concentration induced severe pathogenic changes by H. pylori infection in 5 weeks-old Mongolian gerbils. These results suggested that ethanol-pretreatment before H. pylori inoculation could increase the severity of gastric mucosal inflammation and enhance the colonization of H. pylori. The established ethanol-pretreating animal model would contribute to screen new drugs against H. pylori and be used as an useful tool for various animal experiments with H. pylori strains.

• Biomolecules & Therapeutics
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• 제22권5호
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• pp.420-425
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• 2014

Esophageal reflux of gastric contents causes esophageal mucosal damage and inflammation. Recent studies show that oxygen-derived free radicals mediate mucosal damage in reflux esophagitis (RE). Chlorogenic acid (CGA), an ester of caffeic acid and quinic acid, is one of the most abundant polyphenols in the human diet and possesses anti-inflammatory, antibacterial and anti-oxidant activities. In this context, we investigated the effects of CGA against experimental RE in rats. RE was produced by ligating the transitional region between the forestomach and the glandular portion and covering the duodenum near the pylorus ring with a small piece of catheter. CGA (10, 30 and 100 mg/kg) and omeprazole (positive control, 10 mg/kg) were administered orally 48 h after the RE operation for 12 days. CGA reduced the severity of esophageal lesions, and this beneficial effect was confirmed by histopathological observations. CGA reduced esophageal lipid peroxidation and increased the reduced glutathione/oxidized glutathione ratio. CGA attenuated increases in the serum level of tumor necrosis factor-${\alpha}$, and expressions of inducible nitric oxide synthase and cyclooxygenase-2 protein. CGA alleviates RE-induced mucosal injury, and this protection is associated with reduced oxidative stress and the anti-inflammatory properties of CGA.

• 한국식품영양과학회지
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• 제33권4호
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• pp.659-667
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• 2004

본 실험에서는 흰쥐에서 실험적으로 급성위염, 위궤양 및 십이지장궤양을 유발하고 질경이 에칠아세테이트분획을 투여하여 항위염 및 항위궤양작용에 미치는 영향을 검토하였던 바 다음과 같은 결과를 얻었다. 1. 질경이 에탄올추출물을 n-hexane, chloroform, ethylactae 및 n-butanol로 계통분획하고 농축하여 in vitro에서 항산화력을 측정한 결과 ethyl-acetate분획이 가장 우수하였다. 2. 질경이 에칠아세테이트분획 (PEL 및 PEH)은 HCl-ethanol에 의한 위점막 손상에서 대조군(CON)에 비하여 각 용량별로 55.7% 및 62.1%의 유의적인 항위염작용을 나타냈으며, 특히 고용량투여군인 PEH의 경우 양성 대조약물투여군(60.5%)보다 우수한 효과를 나타냈다. 3. Indomethacin에 의해 유발된 위궤양에서, PEL 및 PEH는 양성 대조약물군인 CMT의 위궤양 억제율(61.6%)에는 다소 미치지 못하였으나 CON에 비하여 유의성 있는 억제 효과를 나타냈다. 4. Shay위궤양에서, 질경이 에칠아세테이트분획 200mg/kg을 십이지장에서 위내로 투여하였을 때 궤양억제율이 37.9%로 CON에 비하여 Shay위궤양을 억제하였으나 유의성있는 효과는 아니었으며 용량을 증량하여 투여한 PEH(400 mg/kg)는 48.9%로 양성 대조약물인 omeprazol를 투여한 OMP의 저해효과(55.6 %)에 근접하였다. 5. 질경이의 에틸아세테이트분획을 용량별로 투여했을 때 위액의 pH가 대조군에 비해 약간의 감소되었으나 정상 범위 내로 유의성은 인정되지 않았고 양성 대조약물군인 OMP는 유의적으로 위액의 pH를 유의성있게 감소시켰다. 위액량 및 총 위산분비량의 경우, 대조군에 비하여 PEL 및 PEH가 각각 33.8%와 38.7%의 감소효과를 나타냈으나 유의성은 없었으며 양성 대조약물인 omeprazol 만큼 뚜렷한 효과는 볼 수 없었다. 6. Pepsin활성에서, 질경이 에틸아세테이트분획과 양성 대조약물투여로 pepsin 활성이 대조군에 비해 각각 약 17%, 22% 및 24%의 활성저해 효과를 나타냈으나 전군에서 유의성 있는 변화는 아니었다. 7 구속ㆍ수침스트레스에 의해 유발된 궤양의 경우, PEL 및 PEH에서도 출혈을 동반한 궤양이 관찰되었으나 CON에 비하여 궤양의 깊이가 다소 얕았지만 유의적인 효과는 아니었다. 양성 약물대조군의 경우 궤양의 형성이 CON과 PEL및 PEH에 비하여 궤양형성의 부분이 다소 적었으나 점상 출혈이 존재하였다. 8. Cysteamine에 의해 유발된 십이지장궤양에서, CMT가 52.2%의 유의한 궤양 억제율을 나타냈고 PEH의 경우 유의성은 없었으나 약 43%의 궤양억제율을 나타냈다.