Wyniki wyszukiwania

1

Interleukin‑1 genotype in periodontitis

100%

Brodzikowska A., Gorska R., Kowalski J.

Archivum Immunologiae et Therapiae Experimentalis

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2019

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tom 67

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nr 6

2

Level of interleukin-1beta and clinical signs after endotoxin injection in stallions

100%

Danek J.

Bulletin of the Veterinary Institute in Puławy

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2002

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tom 46

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nr 2

3

The protective impact of Trans-Cinnamaldehyde (TCA) against the IL-1beta induced inflammation in in vitro osteoarthritis model by regulating PI3K/AKT pathways

86%

Wu J.-R., Zhong W.-J., Chen Z.-D., Zhu B.-Q., Jiang Y.-Y., Wierzbicki P. M.

Folia Histochemica et Cytobiologica

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2020

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tom 58

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nr 4

4

Protective and therapeutic effect of heparin in acute pancreatitis

86%

Ceranowicz P., Dembinski A., Warzecha Z., Dembinski M., Cieszkowski J., Rembiasz K., Konturek S. J., Kusnierz-Cabala B., Tomaszewska R., Pawlik W. W.

Journal of Physiology and Pharmacology. Supplement

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2008

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tom 59

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nr 4

103-125

5

Foxo3a aggravates inflammation and induces apoptosis in IL-1-treated rabbit chondrocytes via positively regulating tenascin-c

86%

Wang F., Wang Q., Zhu M., Sun Q.

Folia Histochemica et Cytobiologica

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2020

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tom 58

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nr 1

6

Interleukin 1beta induces functional prostaglandin E synthase in cultured human umbilical vein endothelial cells

86%

Uracz W., Uracz D., Olszanecki R., Gryglewski R. J.

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 4,1

Prostaglandin endoperoxide H2 (PGH2) is generated from arachidonic acid by either constitutive (COX-1) or inducible (COX-2) cyclooxygenases. In arterial wall PGH2 is converted by PGI2 synthase (PGI-S) to prostacyclin (PGI2), and in platelets by thromboxane synthase (TX-S) to thromboxane (TXA2). Other prostanoids as PGD2, PGF2alpha or PGE2 were believed to arise non-enzymatically from PGH2. Only recently, human prostaglandin E synthase (PGE-S) has been identified and cloned as a membrane bound, microsomal, glutathione-dependent inducible enzyme. Here we demonstrated that interleukin 1ß (IL-1ß) is an inducer of COX-2 and PGE-S in human umbilical vein endothelial cells (HUVEC). Functional expression of PGE-S was measured at the level of specific mRNA by semi-quantitative RT-PCR, PGE-S protein was detected by Western blot in HUVEC, while PGE2 was measured by immunoassay in the supernatant. Actinomycin D, a classical transcription inhibitor, was used to prove that indeed IL-1ß induced the functional PGE-S enzyme. PGE2 generation in HUVEC was inhibited by indomethacin, acetamoniphen and dexamethasone. In conclusion, we found that in cultured endothelial cells IL-1ß induced as evidenced by the appearance of its transcript and its functional enzyme. The induction of endothelial PGE-S and COX-2 appeared to be and their transcripts were induced as fast as one might expect from immediate early genes. It means that IL-1ß-triggered-PGE2 biosynthesis in endothelial cells is probably regulated by induction of both COX-2 and PGE-S. This is way we hypothesise the existence of at least two distinct pools of COX-2: the first selectively coupled to PGE-S and the second one that is coupled to PGI-S yielding the main endothelial product - PGI2.

7

Production of prostacyclin and prostaglandin E2 in resting and IL-1beta-stimulated A549, HUVEC and hybrid EA.HY 926 cells

86%

Olszanecki R., Gebska A., Korbut R.

Journal of Physiology and Pharmacology

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2006

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tom 57

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nr 4

Production of arachidonic acid (AA) metabolites - prostacyclin (PGI2) in large vessels and prostaglandin E2 (PGE2) in microcirculation is intrinsically involved in maintenance of vascular wall homeostasis. EA.hy 926 is a hybrid cell line, is derived by fusion of HUVEC with A549 cells. The aim of this study was to examine the production of prostacyclin and PGE2 in resting and IL-1ß-stimulated EA.ha 926 cells, in comparison with its progenitor cells. Non-stimulated EA.hy 926 cells has been found to produce much lower amounts of prostacyclin than resting HUVEC. Resting hybrid cells produced more PGE2 than prostacyclin, despite they expressed high levels of COX-1 and PGI2 synthase. On the contrary to HUVEC and A549, EA.hy 926 cells did not respond to IL-1ß with COX-2 induction and increase of prostaglandin production, however they did it in response to lysophosphatidylcholine (LPC). The characteristics of EA.hy 926 cells in terms of the pattern of prostanoid formation could facilitate studies on endothelial metabolism and role of these important lipid mediators.

8

Changes in the ultrastructure and functions of immunocompetent cells under the influence of external heating, interleukin 1beta and leukocytic pyrogen

86%

Murzenok P. P., Netukova N. I.

Archivum Immunologiae et Therapiae Experimentalis

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1994

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tom 42

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nr 4

9

IGF-1 stimulates production of interleukin-10 and inhibits development of caerulein-induced pancreatitis

86%

Warzecha Z., Dembinski A., Ceranowicz P., Konturek S. J., Tomaszewska R., Stachura J., Konturek P. C.

Journal of Physiology and Pharmacology

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2003

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tom 54

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nr 4

Insulin-like growth factor-1 (IGF-1) and other growth factors overexpression was reported in acute pancreatitis. Previous studies have shown the protective effect of epidermal growth factor (EGF), Hepatocyte Growth Factor (HGF) and Fibroblast Growth Factor (FGF) in the course of experimental acute pancreatitis. The aim of our studies was to determine the effect of IGF-1 administration on the development of caerulein-induced pancreatitis. Methods: Acute pancreatitis was induced by infusion of caerulein (10 µg/kg/h) for 5 h. IGF-1 was administrated twice at the doses: 2, 10, 50, or 100 µg/kg s.c. Results: Administration of IGF-1 without induction of pancreatitis increased plasma interleukin-10 (IL-10). Infusion of caerulein led to development of acute edematous pancreatitis. Histological examination showed pancreatic edema, leukocyte infiltration and vacuolization of acinar cells. Also, acute pancreatitis led to an increase in plasma lipase and interleukin 1ß (IL-1ß) level, whereas pancreatic DNA synthesis and pancreatic blood flow were decreased. Treatment with IGF-1, during induction of pancreatitis, increased plasma IL-10 and attenuated the pancreatic damage, what was manifested by histological improvement of pancreatic integrity, the partial reversion of the drop in pancreatic DNA synthesis and pancreatic blood flow, and the reduction in pancreatitis-evoked increase in plasma amylase, lipase and IL-1ß level. Protective effect of IGF-1 administration was dose-dependent. Similar strong protective effect was observed after IGF-1 at the dose 2 x 50 and 2 x 100 µg/kg. Conclusions: (1) Administration of IGF-1 attenuates pancreatic damage in caerulein-induced pancreatitis; (2) This effect is related, at least in part, to the increase in IL-10 production, the reduction in liberation of IL-1ß and the improvement of pancreatic blood flow.

10

Effect of ischemic preconditioning on pancreatic regeneration and pancreatic expression of vascular endothelial growth factor and platelet-derived growth factor-A in ischemia-reperfusion-induced pancreatitis

86%

Dembinski A., Warzecha Z., Ceranowicz P., Dembinski M., Cieszkowski J., Pawlik W. W., Tomaszewska R., Konturek S. J., Konturek P. C.

Journal of Physiology and Pharmacology

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2006

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tom 57

|

nr 1

Ischemic preconditioning has been shown to protect several organs from ischemia/reperfusion-induced injury. In the pancreas, protective effect of ischemic preconditioning has been shown against pancreatitis evoked by ischemia/reperfusion, as well as by caerulein. However, the effect of ischemic preconditioning on the course of acute pancreatic is unclear. The aim of our study was to evaluate the influence of ischemic preconditioning on pancreatic regeneration and pancreatic presence of platelet-derived growth factor-A (PDGF-A) and vascular endothelial growth factor (VEGF) in the course of ischemia/reperfusion-induced pancreatitis. Methods: In male Wistar rats, ischemic preconditioning of the pancreas was performed by short-term clamping of celiac artery (twice for 5 min with 5 min interval). Acute pancreatitis was induced by clamping of inferior splenic artery for 30 min followed by reperfusion. Rats were sacrificed 1, 5, 12 h or 1, 2, 3, 5, 7, 9 and 21 days after the start of reperfusion. Severity of acute pancreatitis and pancreatic regeneration were determined by biochemical and morphological examination, expression of growth factors was determined by immunohistochemical analysis. Results: In ischemia/reperfusion-induced pancreatitis, the pancreatic damage reached the maximal range between the first and second day of reperfusion, and was followed by subsequent pancreatic regeneration. Ischemic preconditioning alone caused mild passing pancreatic damage and an increase in plasma concentration of pro-inflammatory interleukin-1 and anti-inflammatory interleukin-10. Ischemic preconditioning applied before ischemia/reperfusion-induced pancreatitis reduced morphological and biochemical signs of the pancreatitis-evoked pancreatic damage and accelerated pancreatic regeneration. This effect was associated with improvement of pancreatic blood flow. Ischemic preconditioning, ischemia/reperfusion-induced pancreatitis and their combination increased the presence of VEGF in acinar and islet cells, and immunostaining for PDGF-A in blood vessels. This effect was maximally pronounced after combination of ischemic preconditioning plus pancreatitis and occurred earlier than after pancreatitis alone. Conclusions: Ischemic preconditioning reduces pancreatic damage and accelerates pancreatic healing in the course of ischemia/reperfusion-induced pancreatitis. This effect is associated with the increase in plasma concentration of anti-inflammatory interleukin-10, improvement of pancreatic blood flow and alteration of pancreatic immunohistochemical expression of PDGF-A and VEGF.

11

Effect of IL-18 on IL-1beta and sIL-1RII production by human neutrophils

86%

Jablonska E., Izycka A., Wawrusiewicz N.

Archivum Immunologiae et Therapiae Experimentalis

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2002

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tom 50

|

nr 2

12

Ghrelin accelerates the healing of oral ulcers in non-sialoadenectomized and in sialoadenectomized rats

72%

Warzecha Z., Kownacki P., Ceranowicz P., Dembinski M., Cieszkowski J., Dembinski A.

Journal of Physiology and Pharmacology

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2013

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tom 64

|

nr 5

13

RhTSG-6 inhibits IL-1beta-induced extracellular matrix degradation and apoptosis by suppressing the p38, and JNK pathways in nucleus pulposus cells

72%

Pei S., Ying J., Zhand Y., Su L., Cheng S., Ruan D.

Folia Histochemica et Cytobiologica

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2020

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tom 58

|

nr 3

14

Investigation of seminal plasma chitotriosidase-1 and leukocyte elastase as potential markers for ‘silent’ inflammation of the reproductive tract of the infertile male - a pilot study

72%

Kratz E. M., Zurawska-Plaksej E., Solkiewicz K., Kokot I., Faundez R., Piwowar A.

Journal of Physiology and Pharmacology

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2020

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tom 71

|

nr 3

15

Prostaglandins and interleukin-1beta in the hypothalamic-pituitary-adrenal response to systemic phenylephrine under basal and stress conditions

72%

Gadek-Michalska A., Bugajski A. J., Bugajski J.

Journal of Physiology and Pharmacology

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2008

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tom 59

|

nr 3

563-575

We investigated the role of interleukin-1ß (IL-1ß) and prostaglandins (PG) in the 1-adrenergic agonist, phenylephrine-induced hypothalamic-pituitary-adrenal axis (HPA) responses under basal and social stress conditions. Male Wistar rats, either control or exposed to crowding stress for 7 days prior to treatment, were used in these experiments. All compounds were injected i.p. Cyclooxygenase COX-1 and COX-2 inhibitors, piroxicam and compound NS-398, IL-1ß and IL-1ß receptor antagonist (IL-1ßRA) were injected 15 min before phenylephrine. Plasma ACTH and serum corticosterone levels were measured 1 h after phenylephrine or IL-1ß injection. Phenylephrine, in respective higher dose administered systemically (0.4 mg/kg i.p.) was almost equally effective as given i.c.v. (30 µg) in stimulating ACTH and corticosterone secretion. Likewise, the extent of the involvement of PG generated by COX-1 and COX-2 in the phenylephrine-induced ACTH and corticosterone secretion was similar after systemic or i.c.v. treatment under both resting and stress conditions. Piroxicam, stronger than compound NS-398, reduced the i.p. phenylephrine-induced ACTH and corticosterone secretion. IL-1ß receptor antagonist (50 µg/kg i.p.) did not significantly affect the inhibitory action of piroxicam on the i.p. phenylephrine-induced ACTH and corticosterone secretion in control rats, but significantly enhanced the inhibition evoked by piroxicam in stressed rats. IL-1ß (2.5 µg/kg i.p.) significantly increased ACTH and corticosterone secretion under basal conditions. Crowding stress for 7 days markedly impaired the IL-1ß-induced ACTH and corticosterone secretion. The mechanism of the stimulatory action of i.p. IL-1ß, which does not cross the blood-brain barrier, may comprise both central and peripheral components of the HPA axis. These results suggest that under basal conditions IL-1ß is not markedly involved in the 1-adrenergic agonist-induced stimulation of the HPA axis activity. During social crowding stress IL-1ß and prostaglandins are significantly involved in this stimulation.

16

Neuroprotective effect of resveratrol against late cerebral ischemia reperfusion induced oxidative stress damage involves upregulation of osteopontin and inhibition of interleukin-1beta

72%

Al Dera H.

Journal of Physiology and Pharmacology

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2017

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tom 68

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nr 1

17

Effects of resveratrol on the expression and DNA methylation of cytokine genes in diabetic rat aortas

72%

Lou X.-D., Wang H.-D., Xia S.-J., Skog S., Sun J.

Archivum Immunologiae et Therapiae Experimentalis

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2014

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tom 62

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nr 4

18

Involvement of cyclooxygenase-1 and cyclooxygenase-2 activity in the therapeutic effect of ghrelin in the course of ethanol-induced gastric ulcers in rats

72%

Warzecha Z., Ceranowicz P., Dembinski M., Cieszkowski J., Ginter G., Ptak-Belowska A., Dembinski A.

Journal of Physiology and Pharmacology

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2014

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tom 65

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nr 1

19

Current status of M1 and M2 macrophages pathway as drug targets for inflammatory bowel disease

72%

Seyedizade S. S., Afshari K., Bayat S., Rahmani F., Momtaz S., Rezaei N., Abdolghaffari A. H.

Archivum Immunologiae et Therapiae Experimentalis

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2020

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tom 68

|

nr 2

20

The role of local and systemic cytokines in patients infected with Clostridium difficile

72%

Czepiel J., Biesiada G., Brzozowski T., Ptak-Belowska A., Perucki W., Birczynska M., Jurczyszyn A., Strzalka M., Targosz A., Garlicki A.

Journal of Physiology and Pharmacology

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2014

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tom 65

|

nr 5

Ograniczanie wyników

Interleukin‑1 genotype in periodontitis

Level of interleukin-1beta and clinical signs after endotoxin injection in stallions

The protective impact of Trans-Cinnamaldehyde (TCA) against the IL-1beta induced inflammation in in vitro osteoarthritis model by regulating PI3K/AKT pathways

Protective and therapeutic effect of heparin in acute pancreatitis

Foxo3a aggravates inflammation and induces apoptosis in IL-1-treated rabbit chondrocytes via positively regulating tenascin-c

Interleukin 1beta induces functional prostaglandin E synthase in cultured human umbilical vein endothelial cells

Production of prostacyclin and prostaglandin E2 in resting and IL-1beta-stimulated A549, HUVEC and hybrid EA.HY 926 cells

Changes in the ultrastructure and functions of immunocompetent cells under the influence of external heating, interleukin 1beta and leukocytic pyrogen

IGF-1 stimulates production of interleukin-10 and inhibits development of caerulein-induced pancreatitis