Melatonin in gastroprotection against stress-induced acute gastric lesions and in healing of chronic gastric ulcers.
The degree of gastric damage following to exposition of the mucosa to noxious agents depends upon a balance between the factors promoting this damage and those activating the natural defense mechanisms. Recent findings, presented in this review, provide evidence that melatonin prevents the formation of acute gastric lesions induced by stress and accelerates healing of chronic gastric ulcers due to increase in the activity of nitric oxide (NO) synthase (NOS)-NO and cyclooxygenase (COX)-prostaglandin E(2) (PGE(2)) systems resulting in the increase of mucosal blood flow and mucosal integrity. Melatonin is produced and released into the circulation by the pineal gland and, in many times larger amounts, by the gastrointestinal tract. Due to its anti-inflammatory and anti-oxidant properties, melatonin may be one of the most efficient protective factors preventing the development of acute gastric damage and accelerating healing of chronic gastric ulcers probably due to reduction in proinflammatory cytokine production, scavenging of the radical oxygen species and activation of COX-PG and NOS-NO systems as well as stimulating the afferent sensory nerves in the brain-gut axis.
Konturek
S J
SJ
Department of Clinical Physiology, Faculty of Medicine, Jagiellonian University Medical College, Cracow, Poland. mpkontur@cyf-kr.edu.pl
Konturek
P C
PC
Brzozowski
T
T
D000818:Animals; D051546:Cyclooxygenase 2 / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D006801:Humans; D008550:Melatonin / Q000378:metabolism / Q000502:physiology*; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D013276:Stomach Ulcer / Q000209:etiology / Q000378:metabolism*; D013312:Stress, Physiological / Q000150:complications* / Q000378:metabolism
D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; D008550:Melatonin; D015232:Dinoprostone