• 제목/요약/키워드: Gastric injury

검색결과 117건 처리시간 0.032초

스트레스와 에탄올로 유발된 mouse의 위점막 손상에 대한 귀비탕의 예방효과 (The Defensive Effect of Keuibi-tang on the Gastric Mucous Membrane of Mouse Injured by Stress and Ethanol)

  • 김학재;최준혁;임성우
    • 대한한의학회지
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    • 제24권1호
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    • pp.155-168
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    • 2003
  • This study was carried out to investigate the effect of Keuibi-tang (KBT) on the injury of gastric mucous membrane by stress and ethanol in mice. The normal group was non-inflammation elicited mice. The two control groups were mice with gastro-inflammation elicited by stress and ethanol. The two sample groups were mice administered KBT before gastro-inflammation elicitation. In the common morphology and histochemical change, the two control groups were observed with various injuries such as hemorrhagic erosion and ulcer, while the sample group was the same as the normal group. In the immunohistochemical change, the distributions of PNA and COX-1 treated with KBT noticeably increased over the control group (P<0.05). The distributions of $NF-{\kappa}B$ p50, COX-2 and TUNEL in the group treated with KBT were noticeably lower than in the control group (P<0.05). The distribution of KBT was the same as the normal group. According to the above results, it is supposed that KBT is applicable to gastritis and gastric ulcer due to stress and alcoholic drinks.

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만성적인 에탄올 섭취로 인한 쥐의 위 조직 손상에서 방사무늬 김(Pyropia yezoensis)의 보호효과 (Protective Effects of Pyropia yezoensis Glycoprotein against Ethanol-induced Chronic Gastric Injury in the Rat)

  • ;최정욱;이민경;김영민;김인혜;남택정
    • 한국수산과학회지
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    • 제47권6호
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    • pp.765-769
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    • 2014
  • We examined the protective effects of Pyropia yezoensis glycoprotein (PYGP) against ethanol-induced gastric damage. The experimental animals were divided into four groups. They were treated with distilled water (control), ethanol alone (EtOH), ethanol + PYGP 150 mg/kg BW (EtOH+150), or ethanol + PYGP 300 mg/kg BW (EtOH+300). The groups were treated for 4 weeks. We measured mitogen-activated protein kinase (MAPK), the apoptotic signaling pathway, and PARP activity in gastric tissues obtained from the rats. Ethanol consumption increased apoptotic signal activity and ERK, JNK, and p38 phosphorylation. PYGP reduced the apoptotic signaling pathway activity and ERK, JNK, and p38 phosphorylation. Furthermore, PYGP regulated Bcl-2 family expression. In light of these findings, PYGP appears to prevent ethanol-induced gastric injury and oxidative stress.

Protective Mechanism of Nitric Oxide and Mucus against Ischemia/Reperfusion-Induced Gastric Mucosal Injury

  • Kim, Hye-Young;Nam, Kwang-Soo;Kim, Kyung-Hwan
    • 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.

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지출환(枳朮丸)의 흰쥐 위(胃) 운동성(運動性)에서 정상 상태 및 위벽 국소손상 후에 대한 효능 (Effect of Jichul-hwan on Gastric Motility in Conscious and Gastric Wall Injured Rats)

  • 이승우;윤상협
    • 대한한방내과학회지
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    • 제29권1호
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    • pp.189-199
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    • 2008
  • Background & Objective : Jichul-hwan(JCH) has been used for the treatment of functional dyspepsia, regarded as a gastric dysmotility disease. We investigated the effects of JCH on gastric motility and its mechanisms of action in rats. Methods : The gastric wall was injured by tracting a part of stomach body in rats. Gastric emptying was measured after administration of normal saline(NS) or JCH in normal rats and gastric wall injured rats. To evaluate the mechanism of JCH under delayed gastric emptying conditions, normal rats were treated with atropine sulfate(1mg/kg, s.c.), quinpirole HCl(0.3mg/kgg, i.p.), $NAME(N^{G}-nitro-L-arginine$ methyl ester, 75mg/kg s.c.) and cisplatin(10mg/kg, i.p.). The gastric slow waves were measured for 30 minutes before and after administration of each solution(NS, JCH). Results : JCH 110.1mg/kg improved gastric emptying for 2 hrs(p=0.014). JCH 110.1mg/kg improved gastric emptying in the gastric wall injured rats(p=0.001). Under the delayed gastric emptying, JCH 110.1mg/kg improved gastric emptying in the group treated with atropine $sulfate(1.83{\pm}0.96$ vs $8.43{\pm}8.46$, p=0.003), but aggravated it with quinpirole $HCl(4.7{\pm}2.9$ vs $1.61{\pm}2.09$, p=0.021). Administration JCH 110.1mg/kg increased EGG power in rats. Conclusions : JCH stimulates gastric motility through the cholinergic pathway, so we expect that it would be effective in the treatment of dysmotility-like functional dyspepsia with low activity of vagus nerve.

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대황(大黃)이 흰쥐의 위점막 손상에 미치는 영향 (Effects of Rhei Rhizoma on Gastric Ulcer in Sprague-Dawley Rats)

  • 김범회
    • 동의생리병리학회지
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    • 제25권1호
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    • pp.71-77
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    • 2011
  • Gastric ulcer has multifactorial etiology, and the development of ulcer is known to be caused by gastric acidity, pepsin secretion, gastric motility and gastric mucosal blood flow. The ulcer results from the tissue necrosis and apoptotic cell death triggered by mucosal ischemia, free radical formation and cessation of nutrient delivery. The gastric mucosa is usually exposed to a wide range of aggressive insults, and has developed efficient mechanisms to repair tissue injury. The apoptotic process of gastric mucosa is triggered by the induction of such proapoptotic gene expression, such as BAX. The Bcl-2 family of proteins plays a pivotal role in the regulation of apoptosis. The maintenance of gastric mucosa integrity depends upon the ratio between cell proliferation and cell death. Stress-inducing factors may affect Bcl-2/BAX ratio and thus the rate of apoptosis through modulation of the expression of both proteins depends upon the experimental model. In addition to the regulation of apoptosis, new vessels have to be generated in order to ensure an adequate supply of oxygen and nutrients to the healing gastric mucosa. This events are regulated by several factors. Among them, such polypeptide growth factors, such as vascular endothelial growth factor (VEGF) regulates essential cell functions involved in tissue healing including cell proliferation and differentiation. The purpose of this study was carried to investigate whether Rhei Rhizoma administration might protect apoptotic cell death and promote angiogenesis in gastric mucosa. Sprague-Dawley rats were randomly divided into 4 groups; normal, saline, cimetidine and Rhei Rhizoma-treated group. The saline, cimetidine and Rhei Rhizoma extracts were orally administrated to each group and gastric ulcer was induced by HCl-EtOH solution. After 1 hour, the stomachs were collected for histological observation and immunohistochemistry. In results, Rhei Rhizoma proves to promote to heal wound in gastric ulcer in conclusion and the significant changes of BAX, Bcl-2 and VEGF quantity in gastric mucosa were observed. These results suggest that Rhei Rhizoma extract may promote incision wound healing and has protective effects on gastric ulcer in rats.

흰쥐의 염증반응에 대한 CW-501027과 CW-501029의 억제효과 (The Inhibitory Effect of CW-501027 and CW-501029 on the Anti-inflammatory Action in Rats)

  • 정지훈;심재호;양성준;민영실;송현주;우재광;김용성;조영래;손의동
    • 약학회지
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    • 제48권6호
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    • pp.317-322
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    • 2004
  • The use of nonsteroidal anti-inflammatory drugs (NSAIDs) is limited by their ability to induce gastrointestinal injury. It has been shown that nitric oxide (NO), similar to pro staglandins (PGs), appears to play an important role in gastric mucosal defence. We hypothesized that NSAIDs contained NO group would be less acutely toxic to the gastric mucosa, but would not interfere with their ability to suppress inflammatory process in rats. We have compared the ulcerogenic and anti-inflammatory effect of CW-501029 (NO-NSAIDs), CW-501027 (NSAIDs) and indomethacin. Both did not change mean blood pressure and heart rates, indicating that they had no side effect on cardiovascular system. We found that CW-501029 increased nitrite/nitrate levels without changing of blood pressure and heart rates. We suggest that it may help gastric mucosal blood flow, the which helps reducing the discomfort in astrointestinal system. Carrageenan-induced PGE2 increase was reduced in a similar tendency when compared CW-501027 or CW-501027 with control in back exudate of rats, but CW-501029 less reduced PGE2 than CW-502027 or indomethacin in gastric tissues. CW-501027 or CW-501029 reduced platelet aggregation. From these results we suggest that CW-501029 may improve the side effect by reduction of short-term gastric injury and less inhibition of PGs synthesis.

경열공 식도절제술을 이용한 부식성 식도협착증의 치료 (Treatment of Corrosive Esophageal Stricture by Transhiatal Esophagectomy and Esophagogastrostomy)

  • 김재범;박창권
    • 대한기관식도과학회지
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    • 제15권1호
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    • pp.35-40
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    • 2009
  • Background: Surgical treatment of corrosive esophageal stricture with colon interposition was very widely used. The colon interposition advantage is low reflux esophagitis risk and preservation of gastric capacity and peristalsis. This procedure was introduced by Orsoni and much improved. But, if stomach injury was minimal, gastric interposition is useful due to simple technique and low complication. Material and Method: Esophageal reconstruction by the transhiatal esophagectomy and intracervical esophagogastrostomy was done in 7 patients of corrosive esophageal stricture at Dong-San medical center from January 1998 to December 2007. Result: There were six female and one male patients raBackground Surgical treatment of corrosive esophageal stricture with colon interposition was very widely used. The colon interposition advantage is low reflux esophagitis risk and preservation of gastric capacity and peristalsis. This procedure was introduced by Orsoni and much improved. But, if stomach injury was minimal, gastric interposition is useful due to simple technique and low complication. Material and Method: Esophageal reconstruction by the transhiatal esophagectomy and intracervical esophagogastrostomy was done in 7 patients of corrosive esophageal stricture at Dong-San medical center from January 1998 to December 2007. Result: There were six female and one male patients ranging from 29 to 69 years of age. The complication was two anastomosis site leakage, one gastric necrosis and one mortality due to bowel strangulation and sepsis. Conclusion: Transhiatal esophagectomy and intracervical esophagogastrostomy is safety and useful method at selection case even though corrosive esophageal resection is debated.

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소건중탕가룡골(小建中湯加龍骨).모려(牡蠣)가 흰쥐의 실험적 위궤양에 미치는 영향 (The Effects of Shogunjungtang-ga-yonggol.morea on Gastric Ulcer)

  • 김태중;이윤희;최우석;박순달;변준석
    • 대한한방내과학회지
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    • 제22권1호
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    • pp.13-20
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    • 2001
  • Object : This study was carried out to examine the effects of Shogunjungtang-ga-younggol morea on gastric ulcers. Methods : In order to study the effects of Shogunjungtang-ga-younggol morea on gastric ulcers. Gastric ulcers were induced in HCI-aspirin in rats. The experiments were done by oral administration and measured by anatohistological features of ulcer lesions, and the changes of the number of parietal cells, chief cells, gastrin and somatostatin- immunoreactive cells. Results : In the Shogunjungtang-ga-younggol morea administrated groups, no gross lesions of ulcer and anatohistologically, just minor injury of gastric mucosa were detected. The number of parietal cells were significantly decreased, and the number of chief cells were significantly increased, in administrated groups. The number of gastrin-immunoreactive cells and somatostatin-immunoreactive cells was significantly increased in administrated groups. Conclusion : According to the results, it is considered that the administration of Shogunjungtang-ga-younggol morea seems to be applicable to the treatment of gastric ulcers.

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Transient receptor potential melastatin type 7 channels are involved in zinc-induced apoptosis in gastric cancer

  • Kim, Byung-Joo
    • Animal cells and systems
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    • 제15권2호
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    • pp.123-130
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    • 2011
  • Transient receptor potential melastatin 7 (TRPM7) channels are novel $Ca^{2+}$-permeable non-selective cation channels that are ubiquitously expressed. Activation of TRPM7 channels has been shown to be involved in the survival of gastric cancer cells. Here we show evidence suggesting that TRPM7 channels play an important role in $Zn^{2+}$- mediated cellular injury. Using a combination of electrophysiology, pharmacological analysis, small interfering RNA (siRNA) methods and cell death assays, we showed that activation of TRPM7 channels augmented $Zn^{2+}$-induced apoptosis of AGS cells, the most common human gastric adenocarcinoma cell line. The $Zn^{2+}$-mediated cytotoxicity was inhibited by the non-specific TRPM7 blockers $Gd^{3+}$ or 2 aminoethoxydiphenyl borate (2-APB) and TRPM7 specific siRNA. In addition, we showed that overexpression of TRPM7 channels in HEK293 cells increased $Zn^{2+}$- induced cell injury. Thus, TRPM7 channels may represent a novel target for physiological disorders where $Zn^{2+}$ toxicity plays an important role.

위식도역류질환과 인후두역류질환의 대한 최신지견 (Update of Pathophysiology in GERO/LPR)

  • 우정수
    • 대한기관식도과학회지
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    • 제16권2호
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    • pp.83-90
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    • 2010
  • The pathophysiology of Gastroesophageal reflux disease (GERD) has been known that it is developed when the offense-primarily the gastric acid-pepsin content of the refluxate-overcomes a 3-tiered esophageal protective defense. consisting of antireflux mechanisms, luminal clearance mechanisms, and tissue resistance. Laryngopharyngeal reflux (LPR), which is known as an extraesophageal variant of GERD, has been considered to be developed by transient lower esophageal sphincter relaxation (TLESR), direct mucosal injury by gastric contents, more sensitive mucosa compared to esophagus, and absence of buffering effect and aggravation of the injury due to pepsin. However, hypothesis of the pathophysiology in both entities are numerous and still lack of understanding for being a theory. There is no conflict that understanding the pathophysiology is necessary for resolving the problems of these diseases and numerous studies and results have been releasing. This review could provide clinicians dealing with GERD and LPR with applicable new information and help for overcoming the clinical obstruction.

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