• The Korea Journal of Herbology
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• v.31 no.1
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• pp.25-31
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• 2016

Objectives : The present study was conducted to evaluate protective effects of Combined Extract of young persimmon fruit and citrus peel (PCM) in Reflux Esophagitis(RE) rats.Methods : Twenty-four Sprague-Dawley (SD) rats were divided four groups and each group had six rats ; Normal group, RE control group, RE group treated PCM 50 ,100 mg/kg body weight group. Reflux esophagitis was induced that tied the pylorus and fundus in SD rats stomach. PCM was administered at 50, 100 mg/kg body weight 2 hrs prior to induction of RE. After 6 hrs, the effects of PCM treated rats were compared with those of normal and control rats. We have performed an analysis such as pH of stomach secretion, oxidative stress biomarkers in serum, and western blot.Results : The increased esophageal mucosa damage by RE was markedly improved by PCM treatment in a dose-dependent manner. Also, the administration of PCM decreased the elevated serum reactive oxygen species (ROS) and peroxynitrite (ONOO^-) in serum. The protein expressions of anti oxidant such as SOD, catalase, GPx exhibited down-regulation by PCM treatment in tissues. And, PCM effectively reduce inflammatory cytokines such as inflammation-related proteins cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), Tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) in RE rats. In addition, NFκB and p-IκBɑ were decreased in PCM-adiministrated RE rats. But there was no difference on stomach secretion pH between reflux esophagitis rats and PCM administration rat group.Conclusions : In conclusion, administration of PCM (50, 100 mg/kg body weight) made esophagus have less inflammation and injury by decreased NFκB path way. These findings suggest that PCM could have Improving effects on reflux esophagitis.

• Journal of Digestive Cancer Research
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• v.10 no.2
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• pp.49-55
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• 2022

Helicobacter pylori (H. pylori) infection is associated with gastroduodenal diseases such as gastritis, peptic ulcer diseases, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. Furthermore, various extragastroduodenal diseases have been suggested to be related with H. pylori infection. Although no single factor has been considered the cause of gastroesophageal reflux disease (GERD), a negative association was found between the prevalence of H. pylori and GERD severity. Additionally, the role of eradication therapy of H. pylori in reflux esophagitis is controversial, and a significant correlation was found between successful H. pylori eradication rate and reflux esophagitis development. H. pylori infection remains an inconclusive and important issue in GERD. Thus, more experimental studies are necessary to elucidate the potential mechanisms.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.6
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• pp.1933-1937
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• 2004

Gastroesophageal reflux disease(GERD) refers to the varied clinical manifestations of reflux of stomach and duodenal contents into the esophagus and is preferable to the 'reflux esophagitis'. Clinical symptoms of reflux esophagitis are heartburn, dysphagia, blood loss, abdominal pain, nocturnal wheezing, coughing, hoarseness. We applied oriental medicines to patient who had reflux esophagitis. we treated them with herb-medication, acupuncture, moxa therapy and aroma therapy for about 2 months. During this period, we observed that symptoms had been improved.

• Archives of Pharmacal Research
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• v.29 no.6
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• pp.484-489
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• 2006

This Study evaluated the inhibitory action of $luteolin-7-O-{\beta}-D-glucuronopyranoside$, luteolin which was isolated from Salix gilgiana leaves, and omeprazole on reflux esophagitis and gastritis in rats. Reflux esophagitis and gastritis were induced surgically and by the administration of indomethacin, respectively. The intraduodenal administration of $luteolin-7-O-{\beta}-D-glucuronopyranoside$ decreased the ulcer index, injury area, gastric volume and acid output, and increased the gastric pH compared with luteolin. $Luteolin-7-O-{\beta}-D-glucuronopyranoside$ significantly decreased the size of the gastric lesions that had been induced by exposing the gastric mucosa to indomethacin. The malondialdehyde content, which is the end product of lipid peroxidation, was increased significantly after inducing of reflux esophagitis. The malondialdehyde content was decreased by $Luteolin-7-O-{\beta}-D-glucuronopyranoside$ but not luteolin or omeprazole. $Luteolin-7-O-{\beta}-D-glucuronopyranoside$ has a more potent antioxidative effect than luteolin. $Luteolin-7-O-{\beta}-D-glucuronopyranoside$ is a promising drug for the treatment of reflux esophagitis and gastritis.

• The Korea Journal of Herbology
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• v.34 no.1
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• pp.117-124
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• 2019

Objective : Chronic acid reflux esophagitis (CARE), one of gastroesophageal reflux disease (GERD) is increasing worldwide. Coptidis rhizoma extract (CRE) is a traditional herb that cures a variety of diseases. This study was conducted to evaluate the protective effect of CR on rats with chronic acid reflux esophagitis. Methods : The antioxidant activities were evaluated through radical scavenging assays using 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2'-azino-bis (3-ethylbenzothiazolin-6-sulfonic acid) (ABTS) radical scavenging assays. CARE was surgically induced in 5-week-old male SD rats by ligating the border between forestomach and glandular portion with a 2-0 silk tie and covering the duodenum using 18-Fr $N{\acute{e}}laton$ catheter. To evaluate the esophageal protective effect of CRE, rats were divided into 3 groups: Nor (normal rats), Veh (chronic acid reflux esophagitis induced rats), CR (chronic acid reflux esophagitis induced rats treated with CRE 200 mg/kg body weight). Results : The administration of CRE significantly prevented the mucosal injury of the esophagus tissue and histological findings improved the esophageal lesion. It has been shown that inflammation is prevented by the increase of antioxidant-related factors (Nrf-2, HO-1, SOD, catalase, and GPx-1/2) through the antioxidant pathway of esophageal tissue. The administration of CRE reduced the increase of serum peroxynitrite ($ONOO^-$) and markedly reduced the protein expression of inflammatory mediator such as $NF-{\kappa}Bp65$, $p-I{\kappa}B{\alpha}$, iNOS, and IL-6. Conclusions : Overall, these results suggest that CRE administration confirmed the protective effect of esophageal mucosa, suggesting that it is a potential treatment for chronic acid reflux esophagitis.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.26 no.4
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• pp.173-180
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• 2023

Purpose: Gastro esophageal reflux disease (GERD) is a burdensome disease affecting many children. A clinical examination is reported to be unreliable to diagnose GERD in children. This study aimed to investigate the relationship between the Pediatric Gastroesophageal Reflux Disease Symptom and Quality of Life Questionnaire (PGSQ) and endoscopic and histopathological findings in children with symptoms suggesting GERD. Changes in the PGSQ score in children with esophagitis as response to one month therapy were recorded as secondary outcome. Methods: This is a prospective cohort study in the pediatric outpatient clinic in an Indonesian tertiary hospital. Children aged 2-17 years old with clinical symptoms suspected of GERD are included in the study. Blinded endoscopic and histopathological examination was performed in all patients before one month proton pump inhibitors (PPI) therapy. The PGSQ information was collected at inclusion and after one month PPI treatment. Results: Fifty-eight subjects were included. Esophagitis was found in 60.9% of subjects according to endoscopy and 58.6% according to histology. There was no significant relationship between the PGSQ score and endoscopic (p=0.781) nor biopsy (p=0.740) examinations. The PGSQ showed a low diagnostic value compared to endoscopy and biopsy (area under the curve [AUC] 0.477, p=0.477, 95% confidence interval [CI] 0.326-0.629 and AUC 0.474, p=0.740 (95% CI 0.321-0.627 respectively). The PGSQ improved significantly post one month of PPI treatment. Conclusion: The PGSQ cannot be used to diagnose esophagitis in children with clinical symptoms suggesting GERD. However, the PGSQ can be used to monitor the treatment response in children with esophagitis.

• Korean Journal of Organic Agriculture
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• v.30 no.1
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• pp.75-87
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• 2022

Reflux esophagitis (RE) is a gastroesophageal reflux disease (GERD) caused by repeated reflux of gastric acid into the esophagus. The present study investigated the protective effect of natural mineral water on esophageal injury induced by gastric acid reflux. The cytotoxicity of mineral water was confirmed using Cell viability, proliferation and cytotoxicity assay kit. The protective effect of mineral water on esophageal injury was investigated in RE rat model. The results showed that no cytotoxicity of mineral water was observed in RAW264.7 cells. Mineral water decreased the ratio of esophageal damage, inhibited the increase of inflammatory-protein expression levels and increased the mucosa protection and tight junction proteins expression level in RE control rat. The results suggest that mineral water may have the potential to protect esophageal damage caused by gastric acid reflux and the potential to alleviate reflux esophagitis.

• The Journal of Internal Korean Medicine
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• v.27 no.4
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• pp.991-998
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• 2006

Gastroesophageal reflux disorder (GERD) refers to reflux of gastric contents into the esophagus leading to esophagitis, reflux symptoms (e.g. heartburn, regurgitation and non-cardiac chest pain) sufficient to impair quality of life, or long term complications. Non-erosive reflux disease (NERD), a subdivision of GERD, is diagnosed when there were some reflux symptoms without esophagitis and mucosal breaks at endoscopy. We report that severe NERD symptoms and lower quality of life which have not responded to more than 6 months' western medical therapy (acid suppression) were successfully improved with traditional oriental medicine.

• Journal of the Korea Convergence Society
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• v.12 no.5
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• pp.255-266
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• 2021

This descriptive survey aimed to investigate the health promotion behaviors of patients with reflux esophagitis and identify the factors influencing it using the health promotion model. The survey was conducted with 178 outpatients diagnosed with reflux esophagitis at C university hospital. Data were analyzed by descriptive statistics, t-test, ANOVA, Pearson's correlation, and multiple regression using SPSS win ver 20. We found that alcohol consumption, BMI, perceived benefit, internal control level, and perceived health status of the patients are significant factors influencing health promotion behavior. The explanatory power was 49%. Therefore, this study is consistent with previous studies that elucidated that changing lifestyle behaviors and obesity control are necessary to alleviate reflux esophagitis. Based on these findings, we propose to develop and apply an educational program for evaluation.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.6
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• pp.319-327
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• 2004

This study was aimed at evaluating the effect of defibrotide on the development of the surgically induced reflux esophagitis, on gastric secretion, lipid peroxidation, polymorphonuclear leukocytes (PMNs) accumulation, polymorphonuclear leukocytes adherence, superoxide anion and hydrogen peroxide production in PMNs, scavenge of hydroxyl radical and hydrogen peroxide, cytokine (interleukin-1 ${\beta}$, tumor necrosis $factor-{\alpha}$) production in blood, and intracelluar calcium mobilization in PMNs. Defibrotide did not inhibit the gastric secretion and not change the gastric pH. Treatment of esophagitis rats with defibrotide inhibited lipid peroxidation, and myeloperoxidase (MPO) in the esophagus in comparison with untreated rats. Defibrotide significantly decreased the PMN adherence to superior mesenteric artery endothelium in a dose-dependent manner, Superoxide anion and hydrogen peroxide production in $1{\mu}M$ formylmethionylleucylphenylalanine (fMLP)- or $0.1{\mu}g/ml$ N-phorbol 12-myristate 13-acetate (PMA)-activated PMNs was inhibited by defibrotide in a dose-dependent fashion. Defibrotide effectively scavenged the hydrogen peroxide but did not scavenge the hydroxyl radical. Treatment of esophagitis rats with defibrotide inhibited interleukin-1 ${\beta}$ production in the blood in comparison with untreated rats, but tumor necrosis $factor-{\alpha}$ production was not affected by defibrotide. The fMLP-induced elevation of intracellular calcium in PMNs was inhibited by defibrotide. The results of this study suggest that defibrotide may have partly beneficial protective effects against reflux esophagitis by the inhibition lipid peroxidation, PMNs accumulation, PMNs adherence to endothelium, reactive oxygen species production in PMNs, inflammatory cytokine production(i.e. interleukin-1 ${\beta}$), and intracellular calcium mobilization in PMNs in rats.