AI Article Synopsis

  • Lactoferrin is a natural immunomodulator with known anti-inflammatory effects, and this study aimed to explore its protective role against esophageal damage from acid reflux in rats.
  • The research involved male Wistar rats and assessed the impact of lactoferrin on gastric acid secretion and esophageal damage after inducing acute acid reflux.
  • Results showed that lactoferrin significantly reduced esophageal damage, improved tissue weight and scores, and lowered proinflammatory markers, indicating its potential as a protective agent against acid reflux in the esophagus.

Article Abstract

Background/aims: The natural immunomodulator lactoferrin is known to possess anti-inflammatory effects. However, there have been no studies examining the mode of action of lactoferrin in protecting the esophageal mucosa against damage. We investigated the effect of lactoferrin on gastric acid secretion and in protecting against acute acid reflux-induced esophagitis in rats.

Methodology: Male Wistar rats aged 8 weeks, weighing 210-240 g, were used for all the experiments. A gastric perfusion system was installed using the method of Ghosh et al. Lactoferrin was administered once via the caudate vein, starting 24 hours before an acute acid reflux (treatment mode), or saline (control). Statistical comparison of the parameters between the two test conditions was performed.

Results: No significant differences in basal or stimulated gastric acid secretion, or in the serum gastrin level were observed between the two test conditions. Esophageal damage was attenuated by lactoferrin in a dose-dependent manner, as reflected by the improvement in the esophageal tissue weight and macroscopic scores. Significant reductions in the histological scores, myeloperoxidase activity and the levels of proinflammatory cytokines, tumor necrosis factor-α and interleukin-1β were also observed following lactoferrin administration.

Conclusions: We concluded that lactoferrin exerts a protective effect against acute acid reflux-induced esophageal damage in rats.

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