Abstract
Gardeniae Fructus 50% EtOH extract (GE) is a traditional herb that has been used to treat a variety of diseases. In this study, we investigate the antioxidant, anti-inflammatory, and antiapoptotic properties of GE on acute reflux-induced esophagitis (RE) model in rats. 2,2′-Azino-bis (3-ethylbenzothiazolin-6-sulfonic acid) (ABTS) and 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging assays were performed to determine the antioxidant activity of GE. GE was given orally at 50 and 100 mg/kg body weight 1h 30 min prior to RE induction. And its effect was assessed in comparison with RE control and normal groups. The administration of the extract of the GE showed remarkable protection of mucosal damage in esophageal tissue, and the histologic observation showed that the gastric lesion was improved. Increased reactive oxygen species (ROS) levels in the serum were diminished by GE treatment. The antioxidative biomarkers including nuclear factor-erythroid 2-related factor 2 (Nrf-2), heme oxygenase-1 (HO-1), superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPX) were significantly increased. GE administration significantly reduced the inflammatory protein expression through MAPK-related signaling pathways and the nuclear factor-kappa B (NF-κB) pathway. These results suggest that GE protects the esophagus mucosal membrane by attenuating oxidative stress and inflammatory response under reflux esophagitis condition through the antioxidant pathway. Therefore, it is suggested that GE may be a potential remedy for the treatment of reflux esophagitis.
Highlights
Reflux esophagitis (RE) is an inflammation of the esophagus caused by reflux of gastric contents due to damage of the lower esophagus
Gardeniae Fructus has been widely used as an herbal medicine for inflammation-related diseases and it has shown various pharmacological abilities such as anti-inflammatory effects and reduction of oxidative stress [13, 14]. ere has been no report on improvement through Gardeniae Fructus 50% EtOH extract (GE) treatment in reflux-induced esophagitis. erefore, we evaluated the antioxidative effects of the Gardeniae Fructus and investigated the effects on the reflux-induced esophagitis rats to explore the improvement effects of oxidative stress-related inflammation
RE is a multifactorial disorder and esophageal pathology most frequently occurring in gastrointestinal disease and has a significant impact on the quality of life and medical costs [21, 22]. e main pathogenesis of RE is complex and diverse, including esophageal mucosal irritability, decreased esophageal capacity, decreased esophageal sphincter function, and gastric motility disorders [23]. e regurgitation of stomach contents is known to cause impairment, inflammation, ulceration, and necrosis of the normal squamous epithelium of the esophagus [24]
Summary
Reflux esophagitis (RE) is an inflammation of the esophagus caused by reflux of gastric contents due to damage of the lower esophagus. Reflux esophagitis causes acidosis and necrosis of the esophageal tissue proliferation of hydrogen ions to the mucosa due to oxidative stress [8]. All of these activities are activated by inflammatory and neutrophils decrease and reactive oxygen species (ROS), resulting in the penetration of active oxygen into all cells and the release of cytokines. Gardeniae Fructus has been widely used as an herbal medicine for inflammation-related diseases and it has shown various pharmacological abilities such as anti-inflammatory effects and reduction of oxidative stress [13, 14]. Gardeniae Fructus has been widely used as an herbal medicine for inflammation-related diseases and it has shown various pharmacological abilities such as anti-inflammatory effects and reduction of oxidative stress [13, 14]. ere has been no report on improvement through Gardeniae Fructus 50% EtOH extract (GE) treatment in reflux-induced esophagitis. erefore, we evaluated the antioxidative effects of the Gardeniae Fructus and investigated the effects on the reflux-induced esophagitis rats to explore the improvement effects of oxidative stress-related inflammation
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