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.
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.
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
/
pp.996-1003
/
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.
Proceedings of the Korean Society of Applied Pharmacology
/
1995.04a
/
pp.92-92
/
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.
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.
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.
Kim, Joo-Il;Kim, Sun-Gil;Kim, Ji-Hoon;Yoon, Chan-Suk;Choi, Ji-Min;Choi, Chan-Hun;Kim, Seon-Jong
Journal of Korean Medicine Rehabilitation
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v.30
no.3
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pp.57-69
/
2020
Objectives The aim of this study was to investigate the inhibitory effect of ChondroT in indomethacin-induced gastric mucosal injury rat model. Methods Sprague-Dawley rats were randomly assigned to intact, control Joins, Celebrex, ChondroT50 and ChondroT200. Indomethacin (25 mg/kg) was used to induce damage to the gastric mucosal injury. ChondroT was administered by orally to inhibit the indomethacin-induced gastric mucosal injury. At the end of the experiment, pH level in stomach, stomach contents volume, tumor necrosis factor-α (TNF-α) level, interleukin-1β (IL-1β) level, prostaglandin E2 (PGE2) level, myeloperoxidase (MPO) activity, erythrocytes, and thrombocytes were measured. Ophthalmologic and histopathological examination was also analyzed. Results pH level in stomach and Stomach contents volume had no difference between Control, PC-Joins, PC-Cele, ChondroT50 and ChondroT200 group. TNF-α level was decreased in PC-Joins, PC-Cele, ChondroT50 and ChondroT200 group and there were no significant difference. IL-1β level was decreased in PC-Joins group and ChondroT200 group compared to control group. PGE2 level had no significant difference between Control, PC-Joins, PC-Cele, ChondroT50 and ChondroT200 group. MPO level and complete blood count level were decreased in PC-Joins, PC-Cele, ChondroT50 and ChondroT200. Symptom score of ophthalmologic examination was decreased in ChondroT50 and ChondroT200 group compared to control group. Conclusion Based on these results, It could be suggested that ChondroT was effective in reducing damage to the gastric mucosal injury. And further study is needed to conduct a rigorous clinical research.
Objectives: This study was carried out to investigate the effects of Sasammaickmoondong-tang (SME) on gastric mucosal lesions induced by indomethacin in mice. Methods: The normal group was no inflammation-induced mice. The control group was gastro-inflammation-induced mice. The sample group was mice administered SME after gastro-inflammation elicitation. Results: In the common morphology and histochemical change, the control group was observed with various injury-mucous surface cell, micro-villi, paneth cell, surface epithelial cell, goblet cell - by hemorrhagic erosion, while the sample group was as same as the normal group. In the immunohistochemical change, the distributions of COX-1, Bcl-2, and BrdU treated with SME were noticeably higher than in the control group (p<0.05). The distributions of TUNEL, NF-B, COX-2, IL-2R-, NK-1.1, ICAM-1, and CD11b/18 in those treated with SME were noticeably lower than in the control group (p<0.05). Finally, the distribution of SBA was the same as in the normal group. Conclusions: According to the above results, it is supposed that Sasammaickmoondong-tang is applicable to gastric mucosal lesions.
Park, Yang-Gyu;Cho, Jeong-Hwi;Choi, Jinyoung;Kim, Youngpil;Lee, Sang-yeob;Park, Ju-Hun;Oh, Hong-Geun
The Korean Journal of Food And Nutrition
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v.34
no.5
/
pp.468-476
/
2021
In recent years, there has been an increase in the morbidity of gastritis in Korea due to lifestyle factors mostly changes in eating habits and stress. Gastritis is more likely to progress to gastric cancer, and therefore it is important to prevent and manage gastritis through lifestyle adjustment and treatment at an early stage. In this study, cabbage, which was found to be effective in gastritis, was mixed and fermented with other crucifer plants such as kale and broccoli to evaluate the overall efficacy of fermented brassica puree on alcoholic acute gastritis. Based on our results, fermented brassica puree alleviated gastric injury induced by 150 mM HCl/60% ethanol. In addition, it was confirmed that PGE2, a gastric mucosal protective factor, was increased, and other positive effects such as an increase of MUC1 and regulation of PKC were observed. The results of this study suggest that fermented brassica puree can relieve acute alcoholic gastritis by regulating PGE and the expression of MUC1, a gene related to mucus secretion, and activating PKC, which is related to mucosal cell activity.
Objective : The present studies investigated the effects of 120Hz high frequency electroacupunctue(EA) on the stress-induced stomach dysfunction in relation to its effect on the level of stress hormone and gastric mucosal damages. The gastric mucosal injury was induced by cold-restraint stress and two acupoints corresponding to Zusanli and Sanyinjiao in man were used. Methods: Cold-restraint stress produced typical gastric lesions in all rats of the stressed groups, but he number of ulcers as well as the mean ulcer diameter were reduced by 120 Hz EA pre-treatment. The cold-restraint stress also induced an increase in catecholamine response involving epinephrine, norepinephrine and dopamine, but an slight decline were observed in EA pre-treated rats compared with cold-restrained rats. Results: The degranulation value of gastric mast cell was significantly higher in cold-restrained rats than in control ones. However, with the significant reduction of degranulation values of gastric mast cells in EA pre-treated rats compared with cold-restrained ones, $PGE_2$ content in the gastric mucosa of EA pre-treated rats was also different from that observed in cold-restrained rats. Cold-restraint stress induced an elevated mRNA expression of pro-inflammatory gene such as cyclooxygenases-2 and tumor necrosis factor(TNF)-${\alpha}$, but these expression were down-regulated in EA pre-treated rats. Immunohistochemecal analysis showed that while the inhibitory-${\kappa}B{\alpha}$ an TNF-${\alpha}$ immunoreaction in the surface epithelium of the stomach tended to increase, both reactions in the EA pre-treated rats showed similar pattern as observed in controls. Conclusions : These results suggest that 120 Hz EA may act as a therapeutical means for gastric mucosal damages through a activation of pituitary adrenal system. it could be concluded that 120 hz high frequency electroacupuncture affords a good protective potential against stress-induce gastrointestinal dysfunction.
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