[Melatonin as a therapeutic factor in gastric ulcer healing under experimental diabetes].
Melatonin (N-acetyl-5-methoxytryptamine) is a hormon secreted mostly by the pineal gland in the brain which maintains the body's circadian rhythm. Interestingly, this indol derivative is produced by enterochromaffin-like cells (ECL) in the gastrointestinal tract (GIT) in amount about 400 fold greater than detected in the pinealocytes. Previous studies revealed that melatonin exerts beneficial action against acute gastric damage induced by stress ethanol, aspirin and ischemia-reperfusion. Hyperglycemia, which is the main symptom of diabetes mellitus, is known to induce mitochondrial dysfunction and endoplasmic reticulum stress, both promoting the generation of reactive oxygen species (ROS). ROS were shown to exhibit higher activity than molecular oxygen under basal conditions due to unpaired electron in its outermost shell of electrons. ROS lead to damage of cellular proteins, nucleic acids and membrane polyunsaturated fatty lipids. In this study, we induced diabetes mellitus by the application of strep. tozocin in presence of gastric ulcers. Male Wistar rats were used in this model. 9 days after gastric ulcers and diabetes mellitus induction, groups of rats were treated with saline or melatonin (20 mg/kg i.g.). At the termination of the experiment, rats were anesthetized, abdomen was opened and gastric blood flow (GBF) was measured. Stomachs were removed for determination of gastric ulcers area by planimetry. Tissue samples were collected for biochemical assays. We demonstrated that melatonin significantly accelerates gastric ulcers healing with and without coexistence of diabetes mellitus. This effect was accompanied by increase of GBF level. Moreover, we observed an increase in superoxide dismutase (SOD) activity and an decrease in lipid peroxidation products concentration within gastric tissue homogenates of animals treated with melatonin, as compared with control group. Melatonin application accelerates gastric ulcers healing with and without presence of diabetes mellitus. We conclude that melatonin can physiologically regulate anti-oxidative enzymes activity and increase GBF level.
Marcin
M
Magierowski
Katarzyna
K
Jasnos
Iwona
I
Brzozowska
Danuta
D
Drozdowicz
Zbigniew
Z
Sliwowski
Elizbieta
E
Nawrot
Urszula
U
Szczyrk
Sławomir
S
Kwiecień
D000818:Animals; D000975:Antioxidants / Q000378:metabolism / Q000494:pharmacology; D003921:Diabetes Mellitus, Experimental / Q000150:complications*; D005753:Gastric Mucosa / Q000098:blood supply* / Q000378:metabolism; D008297:Male; D008550:Melatonin / Q000494:pharmacology* / Q000502:physiology*; D010870:Pineal Gland / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D013276:Stomach Ulcer / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D013482:Superoxide Dismutase / Q000378:metabolism; D014945:Wound Healing / Q000187:drug effects / Q000502:physiology*
D000975:Antioxidants; D017382:Reactive Oxygen Species; D013482:Superoxide Dismutase; D008550:Melatonin