Pinealectomy aggravates acute pancreatitis in the rat

Jaworek, Jolanta; Żwirska-Korczala, K; Szklarczyk, Joanna; Nawrot-Porąbka, Katarzyna; Leja-Szpak, Anna; Jaworek, Andrzej; Tomaszewska, Romana

doi:10.1016/s1734-1140(10)70346-7

Cited by 22 publications

(12 citation statements)

References 47 publications

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“…They found that high endogenous Mel serum levels in the first 24 h after the onset of AP played a protective role in the course of the disease in humans. Moreover, pinealectomy significantly aggravated the histological manifestations of AP [23] on the other hand, Alhan et al [2] assumed that Mel has a limited value on the course of AP as it did not alter pancreatic damage or its mortality rate in rats.…”

Section: Discussionmentioning

confidence: 99%

The protective role of melatonin on L-arginine-induced acute pancreatitis in adult male albino rats

Sadek

Khattab

2017

Folia Morphol

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Background: Acute pancreatitis (AP) is an inflammatory disease that has an incre- Materials and methods: Thirty-six adult male albino rats were used in this study. Animals were divided into four groups; Control group (Group A; n = 6), Mel group (Group B; n = 6), L-arg group (Group C; n = 12) receiving two doses of L-arg injection with 1 h interval in-between, and L-arg+Mel group (Group D; n = 12) receiving Mel 1 h after each L-arg injection. 24 h after the second L-arg injection, the serum levels of amylase (AM), lipase (LP), interleukin-6 (IL-6) and (Folia Morphol 2017; 76, 1: 66-73)

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Section: Discussionmentioning

confidence: 99%

The protective role of melatonin on L-arginine-induced acute pancreatitis in adult male albino rats

Sadek

Khattab

2017

Folia Morphol

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“…Melatonin may also modulate Ca 2+ influx through a non-selective Ca 2+ permeable cation channel in transfected CHO cells [24], and can stimulate Ca 2+ transport across the cellular membranes [25]. In addition, melatonin exerts antioxidant [26,27] and anti-inflammatory properties on the exocrine pancreas [26,[28][29][30].…”

Section: Introductionmentioning

confidence: 99%

Melatonin induces the expression of Nrf2-regulated antioxidant enzymes via PKC and Ca2+ influx activation in mouse pancreatic acinar cells

Santofimia‐Castaño

Ruy

Garcia-Sanchez

et al. 2015

Free Radical Biology and Medicine

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The goal of this study was to evaluate the potential activation of the nuclear factor erythroid 2-related factor and the antioxidant-responsive element (Nrf2-ARE) signaling pathway in response to melatonin in isolated mouse pancreatic acinar cells. Changes in intracellular free Ca(2+) concentration were followed by fluorimetric analysis of fura-2-loaded cells. The activations of PKC and JNK were measured by Western blot analysis. Quantitative reverse transcription-polymerase chain reaction was employed to detect the expression of Nrf2-regulated antioxidant enzymes. Immunocytochemistry was employed to determine nuclear location of phosphorylated Nrf2, and the cellular redox state was monitored following MitoSOX Red-derived fluorescence. Our results show that stimulation of fura-2-loaded cells with melatonin (1 µM to 1 mM), in the presence of Ca(2+) in the extracellular medium, induced a slow and progressive increase of [Ca(2+)](c) toward a stable level. Melatonin did not inhibit the typical Ca(2+) response induced by CCK-8 (1 nM). When the cells were challenged with indoleamine in the absence of Ca(2+) in the extracellular solution (medium containing 0.5 mM EGTA) or in the presence of 1 mM LaCl(3), to inhibit Ca(2+) entry, we could not detect any change in [Ca(2+)](c). Nevertheless, CCK-8 (1 nM) was able to induce the typical mobilization of Ca(2+). When the cells were incubated with the PKC activator PMA (1 µM) in the presence of Ca(2+) in the extracellular medium, we observed a response similar to that noted when the cells were challenged with melatonin 100 µM. However, in the presence of Ro31-8220 (3 µM), a PKC inhibitor, stimulation of cells with melatonin failed to evoke changes in [Ca(2+)]c. Immunoblots, using an antibody specific for phospho-PKC, revealed that melatonin induces PKCα activation, either in the presence or in the absence of external Ca(2+). Melatonin induced the phosphorylation and nuclear translocation of the transcription factor Nrf2, and evoked a concentration-dependent increase in the expression of the antioxidant enzymes NAD(P)H-quinone oxidoreductase 1, catalytic subunit of glutamate-cysteine ligase, and heme oxygenase-1. Incubation of MitoSOX Red-loaded pancreatic acinar cells in the presence of 1 nM CCK-8 induced a statistically significant increase in dye-derived fluorescence, reflecting an increase in oxidation, that was abolished by pretreatment of cells with melatonin (100 µM) or PMA (1 µM). On the contrary, pretreatment with Ro31-8220 (3 µM) blocked the effect of melatonin on CCK-8-induced increase in oxidation. Finally, phosphorylation of JNK in the presence of CCK-8 or melatonin was also observed. We conclude that melatonin, via modulation of PKC and Ca(2+) signaling, could potentially stimulate the Nrf2-mediated antioxidant response in mouse pancreatic acinar cells.

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“…Melatonin treatment was found to promote the spontaneous regeneration process of pancreatic tissue in rats [69] . Jaworek et al [70] have reported that pinealcetomy aggravates AP in the rat. Interestingly, Belyaev et al [71] presented the dynamic changes of endogenous melatonin in the early phase of human AP.…”

Section: Melatoninmentioning

confidence: 99%

Experimental and clinical evidence of antioxidant therapy in acute pancreatitis

Eşrefoğlu

2012

WJG

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Oxidative stress has been shown to play an important role in the pathogenesis of acute pancreatitis (AP). Antioxidants, alone or in combination with conventional therapy, should improve oxidative-stress-induced organ damage and therefore accelerate the rate of recovery. In recent years, substantial amounts of data about the efficiency of antioxidants against oxidative damage have been obtained from experiments with rodents. Some of these antioxidants have been found beneficial in the treatment of AP in humans; however, at present there is insufficient clinical data to support the benefits of antioxidants, alone or in combination with conventional therapy, in the management of AP in humans. Conflicting results obtained from experimental animals and humans may represent distinct pathophysiological mechanisms mediating tissue injury in different species. Further detailed studies should be done to clarify the exact mechanisms of tissue injury in human AP. Herein I tried to review the existing experimental and clinical studies on AP in order to determine the efficiency of antioxidants. The use of antioxidant enriched nutrition is a potential direction of clinical research in AP given the lack of clues about the efficiency and safety of antioxidant usage in patients with AP.

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Pinealectomy aggravates acute pancreatitis in the rat

Cited by 22 publications

References 47 publications

The protective role of melatonin on L-arginine-induced acute pancreatitis in adult male albino rats

The protective role of melatonin on L-arginine-induced acute pancreatitis in adult male albino rats

Melatonin induces the expression of Nrf2-regulated antioxidant enzymes via PKC and Ca2+ influx activation in mouse pancreatic acinar cells

Experimental and clinical evidence of antioxidant therapy in acute pancreatitis

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