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Abstract
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 pro-inflammatory 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.
Highlights
The reflux of gastric acid and stomach contents induces epithelial lesion and cell death in the esophagus, which is associated with inflammatory response caused by inflammatory cell infiltration and pro-inflammatory cytokine expression in damaged tissues [1, 2]
The result that take a view of morphological transformation of cells showed the inflammation reaction on LPS induced Raw 264.7 cells lead to morphological change
The cells pre-treated with geraniin 100 μM showed most similar shape to normal (Fig. 1a)
Summary
The reflux of gastric acid and stomach contents induces epithelial lesion and cell death in the esophagus, which is associated with inflammatory response caused by inflammatory cell infiltration and pro-inflammatory cytokine expression in damaged tissues [1, 2]. A tight junction protein (TJP) in both endothelial and epithelial cells, has barrier and fence functions and is related to GERD. Barrier dysfunction has been demonstrated in inflammatory bowel disease and gastric tissues, and it is associated with TJP such as claudin, occludin, and ZO-1as well as inflammatory cytokines [4, 5]. Claudin-5 protein expression has been demonstrated in different types of mucosa and cells, and its expression was changed by the expression of proinflammatory cytokines [4, 9].
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