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The role of melatonin in gastritis and gastro-esophageal reflux disease

Gastritis is a chronic or acute inflammation of the gastric mucosa. Acute gastritis is sudden inflammation, caused by imbalance in the mucosal mechanisms of defense, represented by the mucus layer and bicarbonate secretion, and gastric acidity, leading to gastric erosion. Chronic gastritis is a gradual inflammation, less aggressive, which lasts in time, generally caused by Helicobacter pylori infection.

The gastro-esophageal reflux disease occurs when stomach acid flows back into esophagus, because of the relaxation of lower esophageal sphincter (LES). It should relax and open only at the food passage, but in some pathological conditions it does not work correctly and lead to reflux. The esophagus does not have the same mechanism of defense of the stomach, so the acid content damages the esophagus mucosa, causing the retrosternal chest pain and acidic sensation in the mouth.

Melatonin is a hormone produced from the pineal gland in response to the alternation to light and dark, regulating the sleep cycle. However, melatonin is produced also in the gastro-intestinal tract by enteroendocrine cells. The amount of melatonin in the stomach after a meal is from 100 to 400 times higher than in the pineal gland, supporting a specific role of melatonin in digestion and that it represents a strategy to treat gastric diseases as gastritis and gastro-esophageal reflux.

  • Melatonin stimulates the bicarbonate secretion

The research from Sjoblom and Flemstrom (2003) shows that the treatment of intestinal epithelial cells with melatonin increases significantly bicarbonate secretion, compared to the control.

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The bicarbonate secretion is fundamental for the gastric mucosa integrity, since it is an element of the mucus and buffers the gastric acid.

  • Melatonin stimulates the nitric oxide and prostaglandins production

Melatonin stimulates the nitric oxide production, which contributes to the mucosa repair, increasing angiogenesis and blood flow, and prostaglandins production, signaling molecules important for the balance of mucus secretion and inhibition of gastric acid secretion (Brzozowska et al., 2002).

  • Antioxidant effect

Melatonin exerts antioxidant effect, protecting the gastric mucosa. In particular, it is a radical scavenger and stimulates the activity of antioxidant molecules, such as superoxide dismutase and glutathione peroxidase (Bonnefont-Rousselot e Collin, 2010).

  • Melatonin inhibits gastric acid secretion and stimulates gastrin secretion

As shown in the figure from Jaworek et al. (2005) research, melatonin reduces the gastric acid secretion, that can be correlated also to the stimulation of prostaglandins production, and increases gastrin secretion. Gastrin is the hormone secreted by the gastric mucosa in consequence of food ingestion, which controls the relaxation of LES, blocking its relaxation during digestion. So, melatonin represents an interesting option to treat gastro-esophageal reflux disease

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  • Melatonin in the treatment of gastro-esophageal reflux disease

In the research of Kandil et al. (2010) it was evaluated the potential therapeutic effect of melatonin in gastro-esophageal reflux disease, comparing its effects to a PPI drug, the most interesting results are reported in the figure.

The researchers compared some parameters of the disease, in healthy controls and in patients before and after the treatment with melatonin or the drug. After 8 weeks of treatment, all the parameters go back to control values in those who received melatonin, meanwhile the drug is effective only of some aspects of the disease. An example: the first parameter, the LES pressure, is not touched at all by the drug, meanwhile the treatment with melatonin shifts its value from 10 to 20.2, when the healthy control il 22.8.

  • Melatonin as preventive agent of gastrointestinal damage induced by NSAID

Thanks to all the mechanisms previously mentioned, melatonin represents a protection toward the gastrointestinal damage induced by NSAID, which are considered one of the major risk factor for gastritis (Sánchez et al., 2020). Since it stimulates prostaglandin secretion, melatonin counteracts the inhibition of cyclooxigenase, the enzyme needed for their synthesis, and since it stimulates mucus secretion, it offers protection to the gastric mucosa against the acid secretion, which is more abundant when NSAID are administered. Moreover, melatonin increases nitric oxide levels, which contributes to tissue repair and, as antioxidant, protect from the ROS coming from the drub metabolism.

In conclusion, melatonin represents a strategy to manage gastritis and gastro-esophageal reflux disease, since it is able to counteract not only symptoms but it acts on the molecular mechanism of the causes.

References

Bonnefont-Rousselot, D., & Collin, F. (2010). Melatonin: action as antioxidant and potential applications in human disease and aging. Toxicology, 278(1), 55-67.

Brzozowska, I., Konturek, P. C., Brzozowski, T., Konturek, S. J., Kwiecien, S., Pajdo, R., … & Hahn, E. G. (2002). Role of prostaglandins, nitric oxide, sensory nerves and gastrin in acceleration of ulcer healing by melatonin and its precursor, L‐tryptophan. Journal of pineal research, 32(3), 149-162.

Jaworek, J., Brzozowski, T., & Konturek, S. J. (2005). Melatonin as an organoprotector in the stomach and the pancreas. Journal of pineal research, 38(2), 73-83.

Kandil, T. S., Mousa, A. A., El-Gendy, A. A., & Abbas, A. M. (2010). The potential therapeutic effect of melatonin in gastro-esophageal reflux disease. BMC gastroenterology, 10(1), 1-9.

Sánchez, A. B., Clares, B., Rodríguez-Lagunas, M. J., Fábrega, M. J., & Calpena, A. C. (2020). Study of melatonin as preventive agent of gastrointestinal damage induced by sodium diclofenac. Cells, 9(1), 180.

Sjöblom, M., & Flemström, G. (2003). Melatonin in the duodenal lumen is a potent stimulant of mucosal bicarbonate secretion. Journal of pineal research, 34(4), 288-293.

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