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Mucosal strengthening activity of central and peripheral melatonin in the mechanism of gastric defense.
J Physiol Pharmacol. 2009 Dec; 60 Suppl 7:47-56.JP

Abstract

This review summarizes the involvement of centrally and peripherally applied melatonin, a major hormone of pineal gland, in the mechanism of gastric mucosal integrity, gastroprotection and ulcer healing. Melatonin was originally shown to attenuate gastric mucosal lesions but the controversy exists in the literature as to whether melatonin derived from the pineal gland, considered as the major source of this indole or rather that locally generated from L-tryptophan within gastric mucosa, plays predominant role in the mechanism of gastrointestinal integrity. Both, intragastric (i.g.) and intracerebroventricular (i.c.v.) administration of melatonin and its precursor, L-tryptophan to rats without or with removed pineal gland by pinealectomy attenuates in the dose-dependent manner the formation of on gastric lesions induced by topical irritants and water immersion restraint stress (WRS). Melatonin accelerated the gastric ulcer healing and this was accompanied by the rise in gastric blood flow (GBF), the plasma melatonin and gastrin levels, the mucosal generation of PGE(2) and luminal NO content. Pinealectomy, which suppresses the plasma melatonin levels, markedly aggravated the gastric lesions induced by WRS. Concurrent supplementation of pinealectomized animals with melatonin or L-tryptophan, the melatonin precursor, attenuated the lesions induced by WRS. Treatment with luzindole, an antagonist of Mel(2) receptors, or with L-NNA, the NO-synthase inhibitor, significantly attenuated melatonin- and L-tryptophan-induced protection and the acceleration of ulcer healing and the accompanying increase in the GBF and luminal content of NO. We conclude that 1) exogenous melatonin and that released from the L-tryptophan attenuate lesions induced by topical irritant such as ethanol and WRS via interaction with MT(2) receptors and due to an enhancement of gastric microcirculation, probably mediated by NO and PG derived from cNOS, iNOS and COX-2 overexpression and activity, and 2) the pineal gland plays an important role in the limitation of WRS-induced gastric lesions and acceleration of ulcer healing via releasing melatonin predominately at night time, that exerts gastroprotective and ulcer healing actions.

Authors+Show Affiliations

Department of Anatomy, Jagiellonian University Medical College, Cracow, Poland. mpbrzozo@cyf-kr.edu.plNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

20388945

Citation

Brzozowska, I, et al. "Mucosal Strengthening Activity of Central and Peripheral Melatonin in the Mechanism of Gastric Defense." Journal of Physiology and Pharmacology : an Official Journal of the Polish Physiological Society, vol. 60 Suppl 7, 2009, pp. 47-56.
Brzozowska I, Ptak-Belowska A, Pawlik M, et al. Mucosal strengthening activity of central and peripheral melatonin in the mechanism of gastric defense. J Physiol Pharmacol. 2009;60 Suppl 7:47-56.
Brzozowska, I., Ptak-Belowska, A., Pawlik, M., Pajdo, R., Drozdowicz, D., Konturek, S. J., Pawlik, W. W., & Brzozowski, T. (2009). Mucosal strengthening activity of central and peripheral melatonin in the mechanism of gastric defense. Journal of Physiology and Pharmacology : an Official Journal of the Polish Physiological Society, 60 Suppl 7, 47-56.
Brzozowska I, et al. Mucosal Strengthening Activity of Central and Peripheral Melatonin in the Mechanism of Gastric Defense. J Physiol Pharmacol. 2009;60 Suppl 7:47-56. PubMed PMID: 20388945.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mucosal strengthening activity of central and peripheral melatonin in the mechanism of gastric defense. AU - Brzozowska,I, AU - Ptak-Belowska,A, AU - Pawlik,M, AU - Pajdo,R, AU - Drozdowicz,D, AU - Konturek,S J, AU - Pawlik,W W, AU - Brzozowski,T, PY - 2009/11/15/received PY - 2009/12/20/accepted PY - 2010/4/15/entrez PY - 2010/4/24/pubmed PY - 2010/8/4/medline SP - 47 EP - 56 JF - Journal of physiology and pharmacology : an official journal of the Polish Physiological Society JO - J Physiol Pharmacol VL - 60 Suppl 7 N2 - This review summarizes the involvement of centrally and peripherally applied melatonin, a major hormone of pineal gland, in the mechanism of gastric mucosal integrity, gastroprotection and ulcer healing. Melatonin was originally shown to attenuate gastric mucosal lesions but the controversy exists in the literature as to whether melatonin derived from the pineal gland, considered as the major source of this indole or rather that locally generated from L-tryptophan within gastric mucosa, plays predominant role in the mechanism of gastrointestinal integrity. Both, intragastric (i.g.) and intracerebroventricular (i.c.v.) administration of melatonin and its precursor, L-tryptophan to rats without or with removed pineal gland by pinealectomy attenuates in the dose-dependent manner the formation of on gastric lesions induced by topical irritants and water immersion restraint stress (WRS). Melatonin accelerated the gastric ulcer healing and this was accompanied by the rise in gastric blood flow (GBF), the plasma melatonin and gastrin levels, the mucosal generation of PGE(2) and luminal NO content. Pinealectomy, which suppresses the plasma melatonin levels, markedly aggravated the gastric lesions induced by WRS. Concurrent supplementation of pinealectomized animals with melatonin or L-tryptophan, the melatonin precursor, attenuated the lesions induced by WRS. Treatment with luzindole, an antagonist of Mel(2) receptors, or with L-NNA, the NO-synthase inhibitor, significantly attenuated melatonin- and L-tryptophan-induced protection and the acceleration of ulcer healing and the accompanying increase in the GBF and luminal content of NO. We conclude that 1) exogenous melatonin and that released from the L-tryptophan attenuate lesions induced by topical irritant such as ethanol and WRS via interaction with MT(2) receptors and due to an enhancement of gastric microcirculation, probably mediated by NO and PG derived from cNOS, iNOS and COX-2 overexpression and activity, and 2) the pineal gland plays an important role in the limitation of WRS-induced gastric lesions and acceleration of ulcer healing via releasing melatonin predominately at night time, that exerts gastroprotective and ulcer healing actions. SN - 1899-1505 UR - https://www.unboundmedicine.com/medline/citation/20388945/Mucosal_strengthening_activity_of_central_and_peripheral_melatonin_in_the_mechanism_of_gastric_defense_ L2 - https://medlineplus.gov/stomachdisorders.html DB - PRIME DP - Unbound Medicine ER -