Protective effect of Rhei Rhizoma on reflux esophagitis in rats via Nrf2-mediated inhibition of NF-κB signaling pathway

Park

et al. 2020

Phytotherapy Research

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Gastroesophageal reflux disease (GERD) is a disease that stomach contents continually refluxing into esophagus causes symptoms and/or complications. The study was working to find natural plant extracts with good effects and small side effects to treat reflux esophagitis (RE). The anti‐inflammatory effects of hexane extract of Magnolia sieboldii (MsHE) were conducted on lipopolysaccharide (LPS)‐stimulated RAW 264.7 macrophage cells. The ameliorative effects of MsHE on esophageal damage in rats induced by gastric acid reflux was explored in vivo. The results showed that MsHE decreased the production of nitric oxide (NO) and expression levels of iNOS, COX‐2 and TNF‐α on LPS‐stimulated RAW 264.7 cells and MsHE treatment ameliorated the rats' esophageal tissue damage induced by gastric acid and inhibited the increase of inflammatory mediators and pro‐inflammatory cytokines by regulating NF‐κB signaling pathway. In addition, MsHE protected the function of barrier of epithelial cells against inflammatory conditions through increasing the expression of tight junctions. Furthermore, liquid chromatography‐mass spectrometry analysis was used for determine the active ingredients contained in MsHE. The results show that MsHE can alleviate experimental rat RE by regulating NF‐κB signaling pathway. In summary, MsHE may be used as a source material of drug candidate for the treatment of RE.

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Ameliorative effects of Magnolia sieboldii buds hexane extract on experimental reflux esophagitis

Park

et al. 2020

Phytotherapy Research

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“…To evaluated protective effects of geraniin on reflux esophagitis rats, experimental rats were orally administrated with geraniin (15 and 30 mg/kg body weight) and ranitidine 30 mg/kg body weight 90 min before the surgery. Then, the rats except for those in the normal control group, were subjected to laparotomies to ligate the pylorus and the junction between the forestomach and the corpus [17], and esophageal damage was induced by gastric acid reflux during the ligation. Our data showed that the esophageal tissue of the RE control group showed tissue damages and hemorrhage induced by inflammation compared to the normal control group (Fig.…”

Section: Changes Of Esophagus Tissue Damage In Acute Re Ratsmentioning

confidence: 99%

Geraniin ameliorate experimental acute reflux esophagitis via NF-κB regulated anti-inflammatory activities in rats

Park

et al. 2019

Appl Biol Chem

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Repeated reflux of gastric acid and stomach contents into the esophagus leads to esophagus damage, including inflammation, ulcer, and hemorrhage in the epithelium. In this study, we aimed to demonstrate the ameliorating effects of geraniin, a phytochemical in the geraniums, on esophagus damage in an acute reflux esophagitis (RE) rat model. The inflammatory effects of geraniinwas measured by nitric oxide (NO) production and pro-inflammatory protein levels in lipopolysaccharide (LPS)-induced RAW 264.7 cells. To evaluate the protective effects of geraniin on damaged esophagus tissue in RE rats, the rats were divided into the following groups: normal control; RE-induced control; RE rats pretreated with geraniin 15 and 30 mg/kg body weight; and RE rats pretreated with ranitidine 30 mg/ kg body weight as a positive control. The lesion area of esophagus was determined by the Image J program, and histological changes were examined by hematoxylin and eosin staining of rat esophageal tissue. The expression of proinflammatory proteins, cytokines, and tight junction proteins involved in esophagus damages was determined using western blotting of esophageal tissue. Geraniin revealed that anti-inflammatory effects against LPS-induced cells by significantly decreasing NO production and iNOS proteins level. Additionally, the results showed that improvement effects of geraniin on esophagus damages in RE induced rats. The expression of inflammatory proteins involved in nuclear factor NF-kB signaling pathways significantly decreased and tight junction protein (claudin-4 and claudin-5) was increased in esophageal tissue. We found the potential of geraniin as source of replacement therapy products source for inflammatory and reflux esophagitis disease.

“…By ligating the pylorus to prevent gastric contents from entering the duodenum and by ligating the forestomach to reduce stomach volume, gastric acid is more likely to re ux into the esophagus [32]. Gastric acid re ux leads to esophageal damage including in ammatory in ltration of esophageal cells and shedding of mucosal epithelial tissue [33]. In addition, the expression levels of in ammatory proteins and pro-in ammatory factors in the esophageal tissue vary depending on degree of esophageal injury and in ammation [34].…”

Section: Discussionmentioning

confidence: 99%

Inhibitory Effects of Camellia Japonica on Cell Inflammation and Acute Rat Reflux Esophagitis

Choo

2020

Preprint

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Background Excessive and continuous inflammation may be the main cause of various immune system diseases. Reflux esophagitis (RE) is a common gastroesophageal reflux disease (GERD). It is an inflammation of the esophagus caused by the reflux of gastric contents to the esophagus due to the dysfunction of the lower esophageal sphincter. Camellia japonica has high medicinal value and has long been used as a traditional herbal hemostatic medicine in China and Korea. Materials and methods Dried C. japonica buds were extracted with 75% ethanol. DPPH and ABTS radical scavenging assay were evaluated according to previous method. The ROS production and anti-inflammatory effects of C. japonica buds ethanol extract (CJE) were evaluated on LPS-induced RAW 264.7 macrophage cells. The protective effects of CJE on RE were conducted in a RE induced Sprague Dawley rat model. Results CJE eliminated over 50% of DPPH and ABTS radical at concentration of 100 and 200 µg/mL, respectively. CJE alleviated changes in cell morphology, reduced production of ROS, NO and IL-1β. Also, down-regulated expression levels of iNOS, TNF-α, phosphorylated NF-κB, IκBα, and JNK/p38/MAPK. CJE reduced esophageal tissue damage ratio (40.3%) and attenuation of histological changes. In addition, CJE down-regulated the expression levels of TNF-α, IL-1β, COX-2 and phosphorylation levels of NF-κB and IκBα in esophageal tissue . Conclusions CJE possesses good anti-oxidation and anti-inflammatory activity, and can improve RE in rats caused by acid reflux. Therefore, CJE may be a natural medicine source with good anti-oxidation and anti-inflammatory effects, and a candidate phytomedicine source for treating RE