• 제목/요약/키워드: gastric mucosa

검색결과 340건 처리시간 0.028초

익위탕(益胃湯)의 Indomethacin유발 위점막 손상에 대한 효과 (The Effects of Ikwitang Extract on Indomethacin-induced Gastric Mucosal Lesions)

  • 백태현;신혜승
    • 대한한방내과학회지
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    • 제25권3호
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    • pp.497-507
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    • 2004
  • This study was carried out to investigate the effects of Ikwitang extract on indomethacin-induced gastric mucosal lesions in mice. Experimental groups were classified into a non-treated group(NM group), a non-administered group(CON group), the Misoprostol-administered group(MI group) and the Ikwitang-extract-administered group(IW group). This study examined the morphological change, distribution of mast cells, mucous surface cells, acid mucose secreted cells, and apoptic cells, BrdU, COX-1, Hsp70, $NF-{\kappa}B\;p50$, PKC, COX-2 and IL-12B of gastric mucosa. Results : The results of this study were as follows: 1. In the Misoprostol-administered group and the Ikwitang-extract-administered group, the hemorrhagic erosion of gastric mucous and infiltrated mast cells decreased. 2. Mucous surface cells and acid mucose secreted cells abserved in the Misoprostol-administered group and the Ikwitang-extract administered group. 3. The distribution of apoptic cells, Hsp70, $NF-{\kappa}B\;p50$, PKC, COX-2, and IL-12B increased in the Control group, but decreased in the Misoprostol-administered group and Ikwitang-extract-administered group. 4. Cells proliferation of gastric mucosa and the COX-l positive cells decreased in the Control group, but increased in the Misoprostol-administered group and the Ikwitang-extract -administered group. The above results suggest the lkwitang extract had beneficial effects on indomethacin induced gastric mucosal lesions.

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인체 및 토끼 위선세포에서 인삼사포닌의 위산분비 매개 신호전달체계에 미치는 영향 (Effects of Ginsenosides on Acid Secretion in Gastric Cells Isolated from Human and Rabbit Gastric Mucosa)

  • 김혜영;김신일;김경환
    • Journal of Ginseng Research
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    • 제22권1호
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    • pp.22-31
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    • 1998
  • Antiulcer effects of ginseng saponin, acidic polysaccharide and methanol extract of Panax ginseng in the patients and experimental animals were reported. Postulated action mechanisms of ginseng were histamine-Ht receptor blocking and increasing gastric blood flow In the present study, the effect of ginsenosides, the biologically active glycosides of ginseng, on gastric acid secretion was examined using gastric cells isolated from human and rabbit gastric mucosa. Ginseng saponin, ginsenoside $Rb_1$, $Rb_2$, $Rg_1$ and $Rh_2$ were tested in unstimulated as well as stimulated gastric cells. Histamine ($10^4$M) and 3-isobutyl-1-methylxanthine ($10^4$M) were used as secretagogues. To investigate the mechanism of ginsenosides on acid secretion, the levels of cAMP and cGMP were monitored in gastric cells. As a result, high concerltration(1mg/ml) of ginseng saponin showed 73-75% of stimulated acid secretion in control gastric cells. However, ginseng saponin had no effect on unstimulated acid secretion and the levels of cGMP and cAMP in gastric cells. Ginsenoside $Rb_1$, $Rb_2$ and $Rh_2$ significantly inhibited stimulated acid secretion. Gastric cGMP levels were increased by all ginsenosides tested while cAMP levels were increased by all ginsenosides in unstimulated state of gastric cells, but increased by ginsenosides ginsenoside $Rg_1$ and $Rh_2$in stimulated state of gastric cells. The results suggest that inhibition of ginseng saponin on gastric acid secretion represents a complex effect of individual ginsenosides, which produce a range of effect on acid secretion. The inhibition site of ginseng saponin on stimulated acid secretion is postulated as post cAMP levels in acid secretary pathway such as protein phosphorylation or proton pump. Nitric oxide may not be involved in the inhibitory effect of ginseng saponin on stimulated acid secretion.

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Magnesium Sulfate Induced Toxicity in Vitro in AGS Gastric Adenocarcinoma Cells and in Vivo in Mouse Gastric Mucosa

  • Zhang, Xulong;Bo, Agula;Chi, Baofeng;Xia, Yuan;Su, Xiong;Sun, Juan
    • Asian Pacific Journal of Cancer Prevention
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    • 제16권1호
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    • pp.71-76
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    • 2015
  • Magnesium sulfate is widely used as a food additive and as an orally administered medication. The aim of this study was to evaluate the possible cytotoxicity of magnesium sulfate on AGS human gastric adenocarcinoma cells and gastric mucosa in mice. A trypan blue exclusion assay was used to determine the reduction in viability of AGS cells exposed to magnesium sulfate, and then effects on cell proliferation were quantified. The role of magnesium sulfate-mediated pro-inflammatory cytokine production in AGS cells was also investigated. mRNA expression for IL-$1{\beta}$, IL-6, IL-8, and TNF-${\alpha}$ was determined by RT-PCR, and secretion of these cytokines was measured by ELISA. Immunohistochemical evaluation of IL-$1{\beta}$, IL-6, and TNF-${\alpha}$ expression was conducted in mouse gastric mucosa. Addition of 3 to 50 mM magnesium sulfate to AGS cells inhibited both cell proliferation and cell viability in a dose-dependent manner. Magnesium sulfate had little effect on production of IL-$1{\beta}$ or IL-6 but significantly inhibited production of IL-8. The animal model demonstrated that magnesium sulfate induced production of IL-$1{\beta}$, IL-6, and TNF-${\alpha}$. These preliminary data suggest that magnesium sulfate had a direct effect on the stomach and initiates cytotoxicity in moderate concentrations and time periods by inhibiting viability a nd proliferation of AGS cells and by regulating expression and/or release of pro-inflammatory cytokines.

Evaluation of the gastroprotective effects of 20 (S)-ginsenoside Rg3 on gastric ulcer models in mice

  • Zhang, Kai;Liu, Ying;Wang, Cuizhu;Li, Jiannan;Xiong, Lingxin;Wang, Zhenzhou;Liu, Jinping;Li, Pingya
    • Journal of Ginseng Research
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    • 제43권4호
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    • pp.550-561
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    • 2019
  • Background: Gastric ulcer (GU) is a common gastrointestinal disease that can be induced by many factors. Finding an effective treatment method that contains fewer side effects is important. 20 (S)-ginsenoside Rg3 is a kind of protopanaxadiol and has shown superior antiinflammatory and antioxidant effects in many studies, especially cancer studies. In this study, we examined the treatment efficacy of 20 (S)-ginsenoside Rg3 on GU. Methods: Three kinds of GU models, including an alcohol GU model, a pylorus-ligated GU model, and an acetic acid GU model, were used. Mouse endothelin-1 (ET-1) and nitric oxide (NO) levels in blood and epidermal growth factor (EGF), superoxide dismutase, and NO levels in gastric mucosa were evaluated. Hematoxylin and eosin staining of gastric mucosa and immunohistochemical staining of ET-1, inducible nitric oxide synthase (NOS2), and epidermal growth factor receptors were studied. Ulcer index (UI) scores and UI ratios were also analyzed to demonstrate the GU conditions in different groups. Furthermore, Glide XP from $Schr{\ddot{o}}dinger$ was used for molecular docking to clarify the interactions between 20 (S)-ginsenoside Rg3 and EGF and NOS2. Results: 20 (S)-ginsenoside Rg3 significantly decreased the UI scores and UI ratios in all the three GU models, and it demonstrated antiulcer effects by decreasing the ET-1 and NOS2 levels and increasing the NO, superoxide dismutase, EGF, and epidermal growth factor receptor levels. In addition, high-dose 20 (S)-ginsenoside Rg3 showed satisfactory gastric mucosa protection effects. Conclusion: 20 (S)-ginsenoside Rg3 can inhibit the formation of GU and may be a potential therapeutic agent for GU.

위 운동성 장애가 동반된 역류성 식도염 환자에 대한 한방단독 치험 1례 (A Clinical Case Report of Endoscopic Reflux Esophagitis with Gastric Dysmotility Treated with Korean Traditional Medical Therapy)

  • 윤상협
    • 대한한방내과학회지
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    • 제37권4호
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    • pp.669-677
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    • 2016
  • Reflux esophagitis is a common disease in developed nations. We describe the case of a female patient with endoscopic reflux esophagitis complicated by gastric dysmotility. Both electrogastrography and enterotachography were performed to detect gastric myoelectrical activity and pyloric sphincter function and evaluate gastric motility. The patient was treated only with herbal medications and general acupuncture, with electrical stimulation of the ST.36 (Zusanli) point, in addition to moxibustion therapy. After each primary and secondary treatment, the therapeutic effect was immediately evaluated. At the final follow-up 5 mon after the end of the secondary treatment, the patient’s general condition was assessed, in addition to the mucosa of the esophagus. At follow up, all the patients’ symptoms had disappeared, and the mucosa of the esophagus had returned to normal. We attributed these therapeutic effects to improved gastric dysmotility. To confirm the usefulness of this treatment method, studies of larger numbers of patients with reflux esophagitis treated with Korean traditional medicine are needed.

Anti-Helicobacter pylori Properties of GutGardTM

  • Kim, Jae Min;Zheng, Hong Mei;Lee, Boo Yong;Lee, Woon Kyu;Lee, Don Haeng
    • Preventive Nutrition and Food Science
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    • 제18권2호
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    • pp.104-110
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    • 2013
  • Presence of Helicobacter pylori is associated with an increased risk of developing upper gastrointestinal tract diseases. Antibiotic therapy and a combination of two or three drugs have been widely used to eradicate H. pylori infections. Due to antibiotic resistant drugs, new drug resources are needed such as plants which contain antibacterial compounds. The aim of this study was to investigate the ability of GutGard$^{TM}$ to inhibit H. pylori growth both in Mongolian gerbils and C57BL/6 mouse models. Male Mongolian gerbils were infected with the bacteria by intragastric inoculation ($2{\times}10^9$ CFU/gerbil) 3 times over 5 days and then orally treated once daily 6 times/week for 8 weeks with 15, 30 and 60 mg/kg GutGard$^{TM}$. After the final administration, biopsy samples of the gastric mucosa were assayed for bacterial identification via urease, catalase and ELISA assays as well as immunohistochemistry (IHC). In the Mongolian gerbil model, IHC and ELISA assays revealed that GutGard$^{TM}$ inhibited H. pylori colonization in gastric mucosa in a dose dependent manner. The anti-H. pylori effects of GutGard$^{TM}$ in H. pylori-infected C57BL/6 mice were also examined. We found that treatment with 25 mg/kg GutGard$^{TM}$ significantly reduced H. pylori colonization in mice gastric mucosa. Our results suggest that GutGard$^{TM}$ may be useful as an agent to prevent H. pylori infection.

오패산(烏貝散)이 HCl-aspirin으로 유발(誘發)된 백서(白鼠)의 위궤양(胃潰瘍)에 미치는 면역조직화학적(免疫組織化學的) 연구(硏究) (The immunohistochemical studies of Opaesan on Gastric ulcer induced by HCl-aspirin in rat)

  • 한상순;한상원;박순달
    • 대한한방내과학회지
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    • 제19권2호
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    • pp.185-207
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    • 1998
  • In order to study the immunohistochemical effects of Opae-san on gastric ulcer induced by HCl-aspirin in rats, experiments were done by oral administration and measure histological features of ulcer lesion, scaning electron microscopic appearance, the changes of numbers of parietal cells, chief cells, gastrin and somatostatin-immunoreactive cells. The obtained results are as follows: 1. Ulcerative lesions were numerously detected in control groups especially in junction of cardiac-fundic gastric mucosa and histologically very severe injury to gastric epithelium were observed too but in the Opae-san administrated groups, no gross lesion of ulcer were detected and histologically minor injury of gastric mucosa were observed. Most slight injuries to gastric mucosa were observed in 5 days after treatment. 2. The numbers of parietal cells were remarkably increased in control group but in Opae-san administrated groups appeared significant decrease compared to control groups. Most remarkably decrease of the numbers of parietal cells compared to control groups were observed in 5 days after treatment. 3. The numbers of chief cells were remarkably decreased in control group but in Opae-san administrated groups appeared significant increase compared to control groups. Most remarkably increase of the numbers of chief cells compared to control groups were observed in 5 days after treatment. 4. The numbers of gastrin-immunoreactive cells were remarkably decreased in control group but in Opae-san administrated groups appeared significant increase compared to control groups. Most remarkably decrease of the numbers of gastrin-immunoreactive cells compared to control groups were observed in 5 days after treatment. 5. The numbers of somatostatin-immunoreactive cells were remarkably decreased in control group but in Opae-san administrated groups appeared significant increase compared to control groups. Most remarkably decrease of the numbers of somatostatin-immunoreactive cells compared to control groups were observed in 5 days after treatment. 6. Scaning electron microscopically, severe denude and degeneration of gastric mucosa were observed in control groups but in Opae-san administrated groups the lesions were remarkably decreased compared to control groups.

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Helicobacter pylori 감염 위염에서의 비만세포 증가와 Stem Cell Factor Receptor (c-kit)의 발현 (Mast Cell Increase and Stem Cell Factor Receptor (c-kit) Expression in Helicobacter pylori-infected Gastritis)

  • 제갈승주
    • 대한임상검사과학회지
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    • 제37권1호
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    • pp.41-46
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    • 2005
  • It is known that mast cells (MCs) are increased in H. pylori-infected gastritis and its increase is mediated by stem cell factor (c-kit ligand). To determine the mechanism of mast cell recruitment and activation by stem cell factor, weinvestigated the expression of stem cell factor receptor (c-kit) in H. pylori-positive and -negative gastric mucosa. Biopsy specimens from 16 H. pylori-negative and 20 positive subjects were examined. H. pylori infection in gastric mucosa was examined by the Warthin-Starry method. MC and c-kit were identified by immunohistochemisty, using a monoclonal antihuman MC tryptase antibody and a polyclonal anti-human c-kit antibody. Densities of MC and c-kit positive cell were measured by a computerized image analysis system. MCs were detected in the lamina propria of both H. pylori-positive and -negative gastric mucosa. Densities of MC and c-kit positive cell were significantly greater in H. pylori-positive than -negative subjects. c-kit was located on the surface of MCs. These results indicate that stem cell factors may be one of the factors involved in mast cell increase and that they activate mast cells by binding with c-kit.

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Gastroprotective effect of zosterin, a pectin from seagrass ZOSTERA MARINA L.

  • Khasina, Eleonora I.;Tiupeleev, Piotr A.;Sgrebneva, Marina N.
    • Advances in Traditional Medicine
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    • 제4권4호
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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.

Comparative effect of silkworm powder from 3 Bombyx mori varieties on ethanol-induced gastric injury in rat model

  • Lee, Da-Young;Cho, Jae-Min;Yun, Sun-Mi;Hong, Kyung-Sook;Ji, Sang-Deok;Son, Jong-Gon;Kim, Eun-Hee
    • International Journal of Industrial Entomology and Biomaterials
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    • 제35권1호
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    • pp.14-21
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    • 2017
  • Gastric ulcer is a clinical symptom characterized by inflammation of the gastric mucosa. Stress and alcohol consumption have been identified as the major cause of gastric ulcer. However, the effects of silkworms on ethanol-induced gastric ulcer have not been studied yet. The mature silkworms that are difficult to eat have become easier to ingest due to recent technological development to make steaming and freeze-drying mature silkworm larval powder (SMSP). In this study, we investigated whether three silkworm varieties, Baekokjam, Golden-silk and Yeonnokjam could alleviate ethanol-induced gastric mucosal damage in vivo. Sprague-Dawley rats pretreated with 3 SMSPs (0.1 or 1 g/kg BW) or normal diet (AIN-76A) were exposed to absolute ethanol (3 g/kg BW, 3 h) by oral gavage. Morphological examination included ulcer index as a measurement of hemorrhages and hematoxylin and eosin staining was performed to analyze the severity of gastric ulcer. Results of macroscopic examination suggested that all 3 SMSPs pretreatment significantly protected gastric mucosa against ethanol-induced damage. Microscopic observations demonstrated significant mucosal erosion and inflammation in ethanol-treated rats, which was abrogated in rats pretreated with 3 SMSPs. In addition, pretreatment with all 3 SMSPs showed significant decreases the expression of pro-inflammatory mediators, IL-6 and cyclooxygenase-2. Among SMSP from 3 varieties of silkworm, preadministration of 1 g/kg Baekokjam SMSP showed the most effective protective effect against ethanol-induced gastric ulcer. These results suggest that Baekokjam SMSP can be a potential gastroprotective agent against ethanol-induced gastric ulcer.