Abstract
Reflux esophagitis, a common gastrointestinal disease, may be induced by duodeno gastroesophageal-reflux, and by duodeno-esophageal reflux (DER), the reflux of the biliary content only. D-002, a mixture of six higher primary alcohols purified from the beeswax, has exhibited gastric and esophageal protection experimentally. The aim of this work was to investigate the effects of D-002 on the esophageal histological changes in rats with DER-induced esophagitis. Rats were randomized into six groups: a negative control and five with DER: a positive control, three D-002- (50, 200 and 400mg/kg, respectively) and one omeprazole (20 mg/kg) group, treated for 14 days. Microscopic studies of esophagus were performed looking for reflux esophagitis indicators, such as basal cell hyperproliferation, papillae elongation, inflammatory cell infiltrates, epithelial erosions and ulcerations. The thickness of esophageal epithelium was measured and leukocytes were counted. Histological characteristics of esophagitis were evaluated. Negative controls had normal esophagus, while positive controls exhibited marked esophagitis. The values of the histological score, thickness of the esophageal epithelium and leukocyte infiltration in the positive control group were higher (p <0.001) than in the negative control. D-002 (50 - 400 mg/kg) reduced significantly (p <0.01) the histological scores versus the positive control group. D-002 lowered significantly the epithelium thickness and abolished (p <0.001) leukocytes infiltration versus the positive control. Compared with the positive control, omeprazole reduced (p <0.01) the histological score, the epithelium thickness and leukocytes infiltration. Repeated doses of D-002 ameliorated the histological changes in rats with DER-induced esophagitis.
Highlights
Reflux esophagitis (RE) is one of the commonest gastrointestinal diseases currently
Esophagitis may be induced by duodenogastroesophageal-reflux (DGER), the flow back of gastric, biliary and pancreatic contents into the stomach; and by duodeno-esophageal reflux (DER), the reflux of the biliary content only. [1 – 3] In patients with gastroesophageal reflux (GER), the concomitant reflux of duodenal content into the lower esophagus can cause mixed RE that may lead to Barett's metaplasia and adenocarcinoma. [4 – 6]
The frequency of animals with esophageal abnormalities corresponding to score 4 in the DER positive control group was higher than in the negative control, while the groups treated with D-002 (50 - 400 mg/kg) or OMP 20 mg/kg had lower frequencies of rats with score 4 as compared to the positive control (p < 0.01)
Summary
Reflux esophagitis (RE) is one of the commonest gastrointestinal diseases currently. RE results from the regurgitation of gastric content that is due to the malfunction of the lower esophageal sphincter (LES) that allows that gastric juice backs to the esophagus. [1 – 3] In patients with gastroesophageal reflux (GER), the concomitant reflux of duodenal content into the lower esophagus can cause mixed (alkaline and acid) RE that may lead to Barett's metaplasia and adenocarcinoma. [12, 13] In patients with gastroesophageal reflux disease (GERD), the concentration of bile acids in the oesophageal reflux is consistent with the degree of oesophageal mucosal damage. [27, 28] Oral acute administration of D-002 reduced GER-induced esophageal lesions and increased oxidative stress in rats, without modifying gastric secretion acidity. D-002, a mixture of six higher primary alcohols purified from the beeswax, [19] has been shown to exert gastroprotection through multiple mechanisms. [20 – 24] Devoid of acid suppressant effect, [20, 21] the mechanisms of the gastroprotective action of D-002 involves the improved quality (content of proteins, glycoproteins, sulphated macromolecules) and increased secretion of gastric mucus, [21,22] anti-inflammatory and antioxidant effects on the gastric mucosa. [23,24] Oral administration of D-002 has demonstrated to reduce hydroxyl radicals, [21] malondialdehyde (MDA) [23,24] and carbonyl groups concentrations, and myeloperoxidase (MPO) activity in the rat gastric mucosa, and to increase the activity of antioxidant enzymes (glutathione peroxidase, superoxide dismutase and catalase). [24] the ability of D-002 for inhibiting 5-lipoxygenase (5-LOX) [25] and to lower concentrations of leukotriene-B4 (LTB4), a gastrotoxic mediator, [26] could contribute to its gastroprotective effects.
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