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1
Content available remote

Dynamics of the melatonin MT1 receptor in the rat parotid gland upon melatonin administration

100%
Isola M., Ekstrom J., Lilliu M. A., Isola R., Loy F.
Journal of Physiology and Pharmacology
|
2016
|
tom 67
|
nr 1
2

Ultrastructural changes in acinar cell mitochondria of the rat pancreas in the course of lead intoxication

100%
Szynaka B., Andrzejewska A.
Folia Histochemica et Cytobiologica. Supplement
|
1996
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tom 34
|
nr 1
3

Pancreatic beta-cell replacement: advances in protocols used for differentiation of pancreatic progenitors to beta-like cells

84%
Ghani M. W., Ye L., Yi Z., Ghani H., Birmani M. W., Nawab A., Cun L. G., Bin L., Mei X.
Folia Histochemica et Cytobiologica
|
2019
|
tom 57
|
nr 3
4
Content available remote

Role of epidermal growth factor receptor transactivation in the activation of cytosolic phospholipase A2 in leptin protection of salivary gland acinar cells against ethanol cytotoxicity

84%
Slomiany B. L., Slomiany A.
Journal of Physiology and Pharmacology
|
2009
|
tom 60
|
nr 2
49-55
A pleiotropic hormone, leptin, secreted into saliva by the acinar cells of salivary glands is an important mediator of the processes of oral mucosal defense. Here, we report on the role of epidermal growth factor receptor (EGFR) transactivation in the signaling events that mediate leptin protection of sublingual salivary gland acinar cells against ethanol cytotoxicity. We show that the protective effect of leptin against ethanol cytotoxicity was associated with the increased EGFR protein tyrosine kinase and cytosolic phospholipase A2 (cPLA2) activity, and characterized by a marked increase in matrix metalloproteinase MMP-9 and arachidonic acid (AA) release, and PGE2 generation. The loss in countering capacity of leptin against ethanol cytotoxicity was attained with JAK inhibitor AG490, Src inhibitor PP2, and EGFR inhibitor AG1478, as well as ERK inhibitor PD98059. Moreover, the agents evoked also the inhibition in leptin-induced up-regulation in cPLA2 activity, AA release, and PGE2 generation. The changes caused by leptin in EGFR phosphorylation, MMP-9, and cPLA2 activation were susceptible to suppression by metalloprotease inhibitor GM6001, but the production of MMP-9 was not affected by EGFR inhibitor AG1478 or PKC inhibitor Ro318220. These findings point to the involvement of MMP-9 in the event of leptin-induced EGFR transactivation that results in the signaling cascade leading to cPLA2 activation and up-regulation in PGE2 generation, thus providing new insights into the mechanism of oral mucosal protection against ethanol toxicity.
5

Inducible nitric oxide synthase immunoreactivity in healthy rat pancreas

84%
Keklikoglu N.
Folia Histochemica et Cytobiologica
|
2008
|
tom 46
|
nr 2
213-217
6

Atrial natriuretic peptide presence in parotid gland of human fetus at 13th week of development and in adult man

84%
Lipari L., Farina E. V., Buscemi M., Gerbino A.
Folia Histochemica et Cytobiologica
|
2013
|
tom 51
|
nr 1
7

The morphology of acinar cells during acute pancreatitis in rats induced by intraductal infusion of peracetate

84%
Jankowski K., Kubasik-Juraniec J., Sledzinski Z., Spodnik J. H., Wozniak M.
Folia Morphologica
|
2004
|
tom 63
|
nr 2
Many experimental models have been created to explain the pathophysiology of acute pancreatitis (AP). Investigations have been undertaken in this laboratory into the influence of strong oxidants introduced into the pancreas retrogradely through the bile-pancreatic duct. In these experiments a potentially toxic metabolite of ethanol-peracetic acid was used to induce AP. Wistar rats were treated with 1 mM and 40 mM peracetate and with a solvent as a control for 1 and 3 hours respectively. After a period of observation the samples of pancreata were examined in a light and electron microscope together with the content of sulphydryl groups as a marker of intracellular oxidative stress. The morphological examination showed profound changes in the histology of the pancreas and also in its subcellular structures, especially in groups 3 and 4 (with a higher concentration of peracetate). The changes included parenchymal haemorrhage and widespread acinar cell necrosis. The level of the sulphydryl groups decreased in the rats treated with peracetate. This suggests that the severity of the disease strongly depends on the intensity of the oxidative stress. The results confirmed the axial role of oxygen-derived free radicals in the pathogenesis of AP.
8
Content available remote

RAS inhibitors decrease apoptosis of acinar cells and increase elimination of pancreatic stellate cells after in the course of experimental chronic pancreatitis induced by dibutyltin dichloride

84%
Madro A., Korolczuk A., Czechowska G., Celinski K., Slomka M., Prozorow-Krol B., Korobowicz E.
Journal of Physiology and Pharmacology. Supplement
|
2008
|
tom 59
|
nr 2
Chronic pancreatitis (CP) is a progressive disease, in which the exocrine function of the gland is gradually lost and fibrosis develops due to repeated episodes of acute pancreatitis. The aim of the study was to investigate the effects of RAS inhibitors on the apoptosis of acinar cells and pancreatic stellate cells (PSCs) elimination in experimental CP induced by dibutyltin dichloride (DBTC). CP was induced by administration of DBTC to the femoral vein. Simultaneously captopril, losartan, enalapril and lisinopril were administered intraperitoneally. The rats were decapitated after 60 days and tissue of pancreas was collected. In rats treated by DBTC the features of inflammatory infiltration, ductal lumen dilatation, fibrosis were found. Strong reactivity with capsase2L and clusterin-ß antibodies was observed in areas of fibrosis. In animals treated with RAS inhibitors inflammatory changes and fibrosis were less severe. In groups of rats treated with DBTC and RAS inhibitors immunoreactivity of capsase2L and clusterin-ß was weak. Positive immunostaining against smooth muscle actine and desmin was observed in the elongated cells (PSC-s). This reaction was weak in groups of rat treated with DBTC and RAS inhibitors. Treatment of CP rats with RAS inhibitors alleviate apoptosis of pancreatic acinar cells and induces PSCs elimination.
9
Content available remote

Activation of peroxisome proliferator-activated receptor gamma impedes Porphyromonas gingivalis lipopolysaccharide interference with salivary mucin synthesis through phosphatidylinositol 3-kinase - ERK pathway

84%
Slomiany B. L., Slomiany A.
Journal of Physiology and Pharmacology
|
2003
|
tom 54
|
nr 1
Peroxisome proliferator-activated receptor (PPAR), a member of the superfamily of nuclear receptor transcription factors, plays a critical role in the regulation of the expression of genes associated with inflammation. Using mucous acinar cells of sublingual salivary gland, we investigated the effect of PPAR activation on the disturbances in salivary mucin synthesis evoked by lipopolysaccharide (LPS) of periodontopathic bacterium, P. gingivalis. Exposure of the acinar cells to the LPS led to a dose-dependent decrease (up to 58.4%) in mucin synthesis, accompanied by a massive enhancement in apoptosis and NO production, and an induction in inducible nitric oxide synthase (NOS-2) activity. Activation of PPAR with a specific synthetic agonist, ciglitazone, prevented in a dose-dependent fashion the LPS-induced reduction in mucin synthesis, and the effect was reflected in a marked decrease in apoptosis, NO generation, and the expression of NOS-2 activity. The impedance by ciglitazone of the LPS-induced changes in mucin synthesis was blocked by PD98059, an inhibitor of extracellular signal regulated kinase (ERK), as well as wortmannin, an inhibitor of phosphatidylinositol 3-kinase (PI3K). Moreover, both agents caused further enhancement in the LPS-induced nitric oxide generation and countered the inhibitory effect of ciglitazone on the LPS-induced upregulation in NOS-2. The findings suggest that the impedance of P. gingivalis LPS inhibition of salivary mucin synthesis by PPAR agonist, ciglitazone, involves activation of ERK pathway by PI3K.
10
Content available remote

Nitric oxide interferes with salivary mucin synthesis: involvement of ERK and p38 mitogen-activated protein kinase

84%
Slomiany B. L., Slomiany A.
Journal of Physiology and Pharmacology
|
2002
|
tom 53
|
nr 3
Nitric oxide (NO), a pluripotent molecule, is an important biological messenger that plays a role in the regulation of tissue homeostasis and pathophysiological processes. Methods: Using sublingual salivary gland acinar cells in culture, we investigated the effect of NO on mucus glycoprotein synthesis, apoptotic processes, and the involvement of extracellular signal-regulated kinase (ERK) and p38 mitogen activated protein kinase (MAPK). Results: Exposure of the acinar cells to NO donor led to a dose-dependent decrease (up to 42.8%) in mucus glycoprotein synthesis, and this effect of NO was accompanied by a marked increase in caspase-3 activity and apoptosis. Inhibition of ERK with PD98059 accelerated (up to 35.4%) the NO-induced decrease in the glycoprotein synthesis, and cause further enhancement in caspase-3 (up to 27.2%) activity and apoptosis (64.9%). On the other hand, blockade of p38 kinase with SB203580 produced a dose-dependent reversal (up to 42%) in the NO-induced reduction in the glycoprotein synthesis, and substantially countered the NO-induced increases in caspase-3 activity (by 62.8%) and apoptosis (by 57.6%). Moreover, caspase-3 inhibitor, Ac-DEVD-CHO, not only blocked the NO-induced increase in caspase-3 activity but also produced an increase in the glycoprotein synthesis. Conclusions: Together, our data indicate that the modulatory influence of NO on salivary mucin synthesis is closely linked to ERK and p38 protein kinase activation, in conjunction with caspase-3 activation and apoptosis.
11
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Content available

Adaptation of pancreas to repeated caerulein-induced pancreatitis in rats

84%
Dembinski A., Warzecha Z., Konturek P. C., Ceranowicz P., Konturek S. J., Tomaszewska R., Stachura J.
Journal of Physiology and Pharmacology
|
1996
|
tom 47
|
nr 3
12
Content available remote

The effect of exogenous apelin on the secretion of pancreatic juice in anaesthetized rats

67%
Kapica M., Jankowska A., Antushevich H., Pietrzak P., Bierla J. B., Dembinski A., Zabielski R.
Journal of Physiology and Pharmacology
|
2012
|
tom 63
|
nr 1
13

Changes in the morphology of the acinar cells of the rat pancreas in the oedematous and necrotic types of experimental acute pancreatitis

67%
Krajewski E., Krajewski J., Spodnik J. H., Figarski A., Kubasik-Juraniec J.
Folia Morphologica
|
2005
|
tom 64
|
nr 4
292-303
Limited experimental models of the oedematous and necrotic types of acute pancreatitis provide some understanding of the pathophysiology of this disease. Wistar rats were treated with cerulein at 10 mg/kg of body weight or with L-arginine at 1.5 or 3 g/kg of body weight in order to induce the oedematous or necrotic type of acute pancreatitis. After the induction period we examined samples of pancreata with light and electron microscopes. Morphological examination showed profound changes in the histology of the pancreas and its acinar cells and subcellular structures, especially in the group of rats which received a higher dose of L-arginine, amounting to 3 g/kg body weight. These included parenchymal haemorrhage and widespread acinar cell necrotic changes. 4-OH-TEMPO successfully prevented morphological deterioration as well as amylase release, suggesting that the severity of the two types of disease strongly depends on the intensity of the oxidative stress. Our results lend support to the assumption that reactive oxygen species play an axial role in the pathogenesis of both types of acute pancreatitis.
14
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

The effect of prostacyclin analogue-iloprost on the pancreas regeneration after cearulein-induced acute pancreatitis in rats

67%
Jurkowska G., Dlugosz J. W., Rydzewska G., Andrzejewska A.
Journal of Physiology and Pharmacology
|
1996
|
tom 47
|
nr 4
15
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

The influence of polyamines synthesis inhibition on pancreas regeneration and phospholipase D activity after acute caerulein induced pancreatitis in rats. Biochemical and ultrastructural study

67%
Jurkowska G., Rydzewska G., Andrzejewska A.
Journal of Physiology and Pharmacology
|
1997
|
tom 48
|
nr 4
16

Epidermal growth factor signalling in rat pancreatic acinar cells

59%
Stryjek-Kaminska D.
Journal of Physiology and Pharmacology. Supplement
|
1998
|
tom 49
|
nr 1
17
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Role of endogenous nitric oxide in the control of exocrine and endocrine pancreatic secretion

59%
Bilski J., Konturek S. J., Bielanski W.
Journal of Physiology and Pharmacology
|
1995
|
tom 46
|
nr 4
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