Abstract
Acute pancreatitis is a disease, which could be manifested as either a mild edematous form or a more severe necrotizing pancreatitis which has a poor prognosis. The etiology and pathogenesis of this ailment is not completely clear. Melatonin is an indoleamine which is produced from L-tryptophan in the pineal gland and in the other tissue including gastrointestinal tract. Both melatonin and its precursor have been demonstrated to protect the pancreas against acute pancreatitis and to attenuate pancreatic tissue damage. In the pancreas melatonin and L-tryptophan activate complex mechanisms which involve direct scavenging of the radical oxygen and nitrogen species, activation of antioxidant enzymes (catalase, superoxide dysmutase, glutation peroxidase), reduction of pro-inflammatory cytokines and prostaglandins, activation of heat shock protein, and a decrease of necrosis and increase of regeneration in the pancreas. There are several arguments for the idea that endogenous melatonin produced in the pineal gland and in the gastrointestinal system could be the part of a native mechanisms for protecting the pancreas against acute damage: 1/ the melatonin precursor L-tryptophan exerts similar protective effect as melatonin, 2/ application of the melatonin receptor antagonist, luzindole aggravates acute pancreatitis, 3/ pinealectomy results in the exacerbation of acute pancreatitis, 4/ low melatonin plasma levels are associated with an increased risk of severe acute pancreatitis.
These observations leads to the idea that perhaps melatonin could be used in clinical trials as supportive therapy in acute pancreatitis.
Keywords: Melatonin, L-tryptophan, acute pancreatitis, antioxidant enzymes, pancreatic protection.
Current Pharmaceutical Design
Title:The Role of Melatonin in Pancreatic Protection: Could Melatonin be Used in the Treatment of Acute Pancreatitis?
Volume: 20 Issue: 30
Author(s): Jolanta Jaworek, Anna Leja-Szpak, Michalina Kot, Andrzej Jaworek, Katarzyna Nawrot-Porbka, Joanna Bonior and Joanna Szklarczyk
Affiliation:
Keywords: Melatonin, L-tryptophan, acute pancreatitis, antioxidant enzymes, pancreatic protection.
Abstract: Acute pancreatitis is a disease, which could be manifested as either a mild edematous form or a more severe necrotizing pancreatitis which has a poor prognosis. The etiology and pathogenesis of this ailment is not completely clear. Melatonin is an indoleamine which is produced from L-tryptophan in the pineal gland and in the other tissue including gastrointestinal tract. Both melatonin and its precursor have been demonstrated to protect the pancreas against acute pancreatitis and to attenuate pancreatic tissue damage. In the pancreas melatonin and L-tryptophan activate complex mechanisms which involve direct scavenging of the radical oxygen and nitrogen species, activation of antioxidant enzymes (catalase, superoxide dysmutase, glutation peroxidase), reduction of pro-inflammatory cytokines and prostaglandins, activation of heat shock protein, and a decrease of necrosis and increase of regeneration in the pancreas. There are several arguments for the idea that endogenous melatonin produced in the pineal gland and in the gastrointestinal system could be the part of a native mechanisms for protecting the pancreas against acute damage: 1/ the melatonin precursor L-tryptophan exerts similar protective effect as melatonin, 2/ application of the melatonin receptor antagonist, luzindole aggravates acute pancreatitis, 3/ pinealectomy results in the exacerbation of acute pancreatitis, 4/ low melatonin plasma levels are associated with an increased risk of severe acute pancreatitis.
These observations leads to the idea that perhaps melatonin could be used in clinical trials as supportive therapy in acute pancreatitis.
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Cite this article as:
Jaworek Jolanta, Leja-Szpak Anna, Kot Michalina, Jaworek Andrzej, Nawrot-Porbka Katarzyna, Bonior Joanna and Szklarczyk Joanna, The Role of Melatonin in Pancreatic Protection: Could Melatonin be Used in the Treatment of Acute Pancreatitis?, Current Pharmaceutical Design 2014; 20 (30) . https://dx.doi.org/10.2174/1381612819666131119105019
DOI https://dx.doi.org/10.2174/1381612819666131119105019 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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