• Title/Summary/Keyword: gastric injury

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Efficacy of Brown Seaweed Hot Water Extract Against Hcl-ethanol Induced Gastric Mucosal Injury in Rats

  • Raghavendran Hanumantha Rao Balaji;Sathivel Arumugam;Devaki Thiruvengadam
    • Archives of Pharmacal Research
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    • v.27 no.4
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    • pp.449-453
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    • 2004
  • Effect of pre-treatment with hot water extract of marine brown alga Sargassum polycystum C.Ag. (100 mg/kg body wt, orally for period of 15 days) on HCI-ethanol (150 mM of HCI-etha-not mixture containing 0.15 N HCI in $70\%$ v/v ethanol given orally) induced gastric mucosal injury in rats was examined with respect to lipid peroxides, antioxidant enzyme status, acid/pepsin and glycoproteins in the gastric mucosa. The levels of lipid peroxides of gastric mucosa and volume, acidity of the gastric juice were increased with decreased levels of antioxidant enzymes and glycoproteins were observed in HCI-ethanol induced rats. The rats pre-treated with seaweed extract prior to HCI-ethanol induction reversed the depleted levels of antioxidant enzymes and reduced the elevated levels of lipid peroxides when compared with HCI-ethanol induced rats. The levels of glycoproteins and alterations in the gastric juice were also maintained at near normal levels in rats pre-treated with seaweed extract. The rats given seaweed extract alone did not show any toxicity, which was confirmed by histopathological studies. These results suggest that the seaweed extract contains some anti-ulcer agents, which may maintain the volume/acidity of gastric juice and improve the gastric mucosa antioxidant defense system against HCI-ethanol induced gastric mucosal injury in rats.

Protective Effect of Taurine on Indomethacin-induced Gastric Mucosal Injury

  • Son, Miwon;Kim, Hee-Kee;Kim, Won-Bae;Yang, Junnick;Kim, Byong-Kak
    • Archives of Pharmacal Research
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    • v.19 no.2
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    • pp.85-90
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    • 1996
  • It has been suggested that oxygen-derived free radicals play an important role in the pathophysiology of acute gastric ulceration induced by NSAIDs and ischemia-reperfusion. Taurine is hypothetized to exert its protective effect on NSAIDs-induced gastric injury by its antioxidant properties. Protective effect of taurine on indomethacin-induced gastric mucosal lesion and its protection mechanism were investigated. Intragastric administration of 25 mg/kg of indomethacin induced hemorrhagic lesions on the glandular stomach in rats. Pretreatment with 0.25 or 0.5 g/kg of taurine one day before or for 3 days significantly reduced the gastric lesion formation and inhibited the elevation of lipid peroxide level in gastric mucosa. The luminol-dependent chemiluminescence of rat peritoneal neutrophils increased immediately after treatment of FMLP or indomethacin. Taurine (5-20 mM) inhibited chemiluminescence of neutrophils activated by FMLP. Human neutrophils (polymorphonuclear leukocytes) significantly adhered to the confluent monolayer of human umbilical vein endothelial cells (HUVEC) after coincubation with indomethacin. This neutrophil adhesion induced by indomethacin to HUVEC was prevented by taurine in a dose-dependent manner. These results indicate that the protective effect of taurine against NSAIDs-induced gastric mucosal injury is due to its antioxidant effect, which inhibits lipid peroxidation and neutrophil activation.

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Palmul-tang, a Traditional Herbal Formula, Protects against Ethanol-induced Acute Gastric Injury in Rats

  • Shin, In-Sik;Lee, Mee-Young;Seo, Chang-Seob;Lim, Hye-Sun;Kim, Jung-Hoon;Jeon, Woo-Young;Shin, Hyeun-Kyoo
    • The Journal of Korean Medicine
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    • v.32 no.6
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    • pp.74-84
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    • 2011
  • Objectives: Palmul-tang (hachimotsu-to in Japanese and bawu-tang in Chinese) is a mixture of eight herbs. It is traditionally used for the treatment of anemia, anorexia, general weakness, and female infertility in China, Japan, and Korea. In this study, we investigated the protective effects of Palmul-tang water extract (PTE) against ethanol-induced acute gastric injury in rats. Material and Methods: Acute gastric lesions were induced by intragastric administration of 5mL/kg body weight of absolute ethanol to each rat. Control group rats were given PBS orally and the ethanol group (EtOH group) received absolute ethanol (5mL/kg) by oral gavage. The positive control group and the PTE group were given oral doses of omeprazole (50mg/kg) or PTE (400mg/kg), respectively, 2 h prior to the administration of absolute ethanol. The stomach of each animal was excised and examined for gastric mucosal lesions. To confirm the protective effects of PTE, we evaluated the degree of lipid peroxidation, the level of reduced glutathione (GSH), and the activities of the antioxidant enzymes catalase, glutathione-S-transferase, glutathione peroxidase, and glutathione reductase in the stomach. Results: PTE reduced ethanol-induced hemorrhage and hyperemia in the gastric mucosa. PTE reduced the increase in lipid peroxidation associated with ethanol-induced acute gastric lesions and increased mucosal GSH content and the activities of antioxidant enzymes. Conclusion: These results indicate that PTE protects gastric mucosa against ethanol-induced acute gastric injury by increasing antioxidant status. We suggest that PTE could be developed as an effective drug for the treatment of acute gastric injury.

Repeated gastric dilatations leading to fatal abdominal compartment syndrome in a patient with bulimia nervosa

  • Han, Seung Baik;Durey, Areum;Lee, Seung Jae;Seo, Young Ho;Kim, Ji Hye
    • Journal of The Korean Society of Emergency Medicine
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    • v.29 no.5
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    • pp.551-556
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    • 2018
  • Cases of repeated acute gastric dilatations after binge eating in one patient are rarely reported. We report here a case of repeated acute gastric dilatations in a 22-year-old woman with bulimia nervosa. Her repeated acute gastric dilatations seem to have been related to superior mesenteric artery syndrome. On her last visit due to acute gastric dilatation, she underwent emergency gastric decompression surgery because of abdominal compartment syndrome; however, she eventually died because of ischemia reperfusion injury. Emergency physicians should be aware of the need to manage acute gastric dilatation in patients with eating disorder and should pay attention to the signs and distinctive clinical features of abdominal compartment syndrome.

PROTECTIVE EFFECT OF TAURINE ON INDOMETHACIN-INDUCED GASTRIC MUCOSAL INJURY

  • Miwon Son;Kim, Hee-Kee;Kim, Won-Bae;Junnick Yang;Kim, Byong-Kak
    • Proceedings of the Korean Society of Applied Pharmacology
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    • 1995.04a
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    • pp.92-92
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    • 1995
  • It has been suggested that oxygen-derived free radicals have an important role in the pathophysiology of acute gastric ulceration induced by NSAIDs and ischemia-reperfusion. Taurine is hypothetized to exert its protective effect on NSAIDS-induced gastric injury by its antioxidant properties, Protect ive effect of taurine on indomethacin-induced gastric mucosal lesion and its protective mechanism were investigated. Intragastric administration of 25 mg/kg of indomethacin induced hemorrhagic lesions on the glandular stomach in rats, Pretreatment with 0.25 g/kg of taurine for 3 days significantly reduced the gastric lesion formation and Inhibited the elevation of lipid peroxide level In gastric mucosa. Both resting and FMLP-induced luminol-dependent chemiluminescence of rat peritoneal neutrophils increased immediately after treatment of indomethacin. 5-20mM of taurine inhibited chemiluminescence of neutrophils activated by indomethacin and/or FMLP. Human neutrophils (polymorphonuclear leukocytes) significantly adhered to confluent monolayer of human umbilical vein endothelial cells(HUVEC) after coincubation with aspirin or indomethacin. Also taurine prevented neutrophil adhesion induced by these drugs to HUVEC in dose-dependent manner. These results indicate that the protective effect of taurine against NSAIDS-induced gastric mucosal Injury is due to its antioxidant effect, which inhibits lipid peroxidation and neutrophil activation.

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The Effects of Processed Garlic on Gastric Mucosa Injury in Rats (흰쥐 위점막 손상에 대한 가공마늘의 효과)

  • 서광희
    • The Korean Journal of Food And Nutrition
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    • v.7 no.3
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    • pp.223-231
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    • 1994
  • This study was designed to investigate the effects of Garlic Jug A Jii, a popular processed food for Korean was given of HCI-ethanol in rats as experimental Model. Oral administration HCI-ethanol to fasted rats produced extensive necrosis in the gastric mucosa. Pretreatment with garlic juice and 3 week stored Garlic Jang A Jii juice prevented such necrosis and the effects were dose-dependent. The effects of garlic Jang A Jii juice comparing with raw garlic juice were reduced but statiscally significant differences were not found. 5 week-stored Garlic Jang A Jii was inhibited the formation of gastric mucosal injury. Comparing with garlic Jug A Jii for 3 weeks, while garlic Jang A Jii juice and 1 : 10 diluted garlic Jang A Jii juice did not show significant shifts but the effects of 1 100 diluted garlic Jang A Jii was decreased. Oral administration of disulfide prevented the gastric mucosa injury whereas sulfhydryl blockers such as N-ethylmaleimie and indomethacin was decreased on gastric mucosa protective effect. The content of diallyl disulfide was 1.41mg% in raw garlic, 0.96mg% in garlic Jang A Jii for 3 weeks. The content of diallyl disulfide was gradually reduced according to the elapse of storage period.

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Protective effects and mechanism of coenzyme Q10 and vitamin C on doxorubicin-induced gastric mucosal injury and effects of intestinal flora

  • Zhao, Xiaomeng;Feng, Xueke;Ye, Nan;Wei, Panpan;Zhang, Zhanwei;Lu, Wenyu
    • The Korean Journal of Physiology and Pharmacology
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    • v.25 no.4
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    • pp.261-272
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    • 2021
  • Doxorubicin (Dox) is widely used to the treatment of cancer, however, it could cause damage to gastric mucosa. To investigate the protective effects and related mechanisms of coenzyme Q10 (CoQ10) and vitamin C (VC) on Dox-induced gastric mucosal injury, we presented the survey of the 4 groups of the rats with different conditions. The results showed Dox treatment significantly induced GES-1 apoptosis, but preconditioning in GES-1 cells with VC or CoQ10 significantly inhibited the Dox-induced decrease and other harm effects, including the expression and of IκKβ, IκBα, NF-κB/p65 and tumor necrosis factor (TNF-α) in GES-1 cells. Moreover, high-throughput sequencing results showed Dox treatment increased the number of harmful gut microbes, and CoQ10 and VC treatment inhibited this effect. CoQ10 and VC treatment inhibits Dox-induced gastric mucosal injury by inhibiting the activation of the IkKB/IκBα/NF-κB/p65/TNF-α pathway, promoting anti-inflammatory effects of gastric tissue and regulating the composition of the intestinal flora.

Chemical Composition of Artemisia argyi Extract (RW0117) and Protective Effects against Gastric Lesions in vivo

  • Lee, Jin Woo;Park, Se Hoon;Jegal, Chang Min;Choi, Keun Young;Jung, Hye Young;Choi, Jung A;Lee, Chan Kyu;Kim, Ho Kyong;Lee, Jung Suk;Lee, Il Kyun
    • Natural Product Sciences
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    • v.26 no.4
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    • pp.268-278
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    • 2020
  • In this study, we investigated the chemical profile and effects of RW0117 (Artemisia argyi 65 .5 % ethanol extract) on gastric lesions in rats. We optimized and validated a method to obtain the chemical profile of RW0117. We then investigated the antioxidant and anti-inflammatory effects in vitro, and the protective effects on gastric lesions in vivo. The IC50 of 2,2-diphenyl-1-picrylhydrazyl free radical scavenging considering the antioxidant effects of RW0117 was 166.55 ㎍/mL, and the IC50 of nitric oxide scavenging considering the anti-inflammatory effects was 41.16 ㎍/mL. Oral administration of RW0117 at lower concentrations (25, 50, 100 mg/kg) had similar or greater effects than the daily intake conversion concentration (115mg/kg) of a health functional food (Avexol®) in the acetic acid-induced ulcer and the ethanol-induced gastric injury rat models. In addition, oral administration of RW0117 increased the expression of prostaglandin E2, which enhances the protective effect in the gastric mucosa in the ethanol-induced gastric injury rat model. These results suggest that RW0117 may have potential therapeutic uses in the protection of the gastric mucosa.

Protective Effect of Astaxanthin Produced by Xanthophyllomyces dendrorhous Mutant on Indomethacin-Induced Gastric Mucosal Injury in Rats

  • Kim, Jeong-Hwan;Choi, Seok-Keun;Lim, Wang-Jin;Chang, Hyo-Ihl
    • Journal of Microbiology and Biotechnology
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    • v.14 no.5
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    • pp.996-1003
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    • 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.

The Management of Pancreatic Fistula Complicated by Gastric Fistulation Following Emergency Splenectomy

  • Huei, Tan Jih;Lip, Henry Tan Chor;Thou, Chow Sing;Mohamad, Yuzaidi;Alwi, Rizal Imran
    • Journal of Trauma and Injury
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    • v.33 no.1
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    • pp.43-47
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    • 2020
  • Pancreatic and gastric fistulas are rare complications of emergency splenectomy, and it is extremely rare for a pancreatic fistula to be further complicated by a fistulation into the stomach. Here, we present a case of pancreatogastric fistula in a 60-year-old man who experienced polytrauma due to a blunt mechanism. He underwent emergency splenectomy for splenic injury and developed a pancreatic fistula as a complication. A percutaneous endoscopic procedure was performed to drain the fistula, after which he developed a pancreatogastric fistula as a further complication. A double-pigtail stent was inserted via gastroscopy into the fistula tract to allow internal drainage of the pancreatic collection into the stomach cavity. When a pancreatic fistula is complicated by gastric fistulation, endoscopic stenting of the pancreatogastric fistula tract for internal drainage is an effective treatment option.