Wyniki wyszukiwania - AGRO

1

Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik

Gastric cytoprotective activity of endogenous 5-HT

100%

Ciurzynska G., Dzierzkowska J., Maslinski S.

Journal of Physiology and Pharmacology

|

1994

|

tom 45

|

nr 4

2

Occurrence of prostaglandins and other eicosanoids in parasites and their role in host-parasite interaction

100%

Szkudlinski J.

Wiadomości Parazytologiczne

|

2000

|

tom 46

|

nr 4

Prostaglandins have been already pretty well rccognized as metabolic regulators in vertebebrata tissues mainly in mammals. Less reports concerned the occurrence of prostaglandins in invertebrates. In the present review we summarise literature data about the presence of prostaglandins and other eicosanoids in various groups of parasites and their possible role in hostparasite interaction. Prostaglandins have also been found in very primitive organisms as bacteria, varions plants and protozoa. We summarise that prostaglandins seem to be a very ancient group, going back to the roots of evolution. They are as universal in cell physiology as DNA in genetics. In host-parasiter eicosanoids also parasitic origin, play an important role as a modulators of hosts immune responsiveness.

3

Prostaglandin-J2 induces the endothelial synthesis of IL-8 independently of PPARgamma activation

100%

Jozkowicz A., Huk I., Nigisch A., Grzenkowicz J., Podhajska A., Weigel G., Dulak J.

Cellular and Molecular Biology Letters

|

2002

|

tom 07

|

nr Suppl.

4

Role of nitric oxide in the nicotine-induced pituitary-adrenocortical response

100%

Gadek-Michalska A., Bugajski J.

Journal of Physiology and Pharmacology

|

2004

|

tom 55

|

nr 2

Nitric oxide (NO) is a major signaling molecule and biological mediator of the hypothalamic-pituitary-adrenal (HPA) axis. We investigated the role of NO formed by endothelial (e), neuronal (n) and inducible (i) nitric oxide synthase (NOS) in the stimulatory effect of nicotine on the HPA axis in rats under basal conditions. Also possible interaction of NOS systems with endogenous prostaglandins (PG) in that stimulation was assessed. NOS and cyclooxygenase inhibitors were administered i.p. 15 min prior to nicotine (2, 5 mg/kg i.p.). Plasma ACTH and serum corticosterone levels were measured 1 h after nicotine injection. NOS blockers given alone did not markedly affect the resting ACTH and corticosterone levels. L-NAME (2-10 mg/kg), a broad spectrum NOS inhibitor considerably and dose dependently enhanced the nicotine-induced ACTH and corticosterone secretion. L-NNA (2 mg/kg) and 7-nitroindazole (7-NI 20 mg/kg), neuronal NOS inhibitors in vivo also significantly augmented the nicotine-induced ACTH and corticosterone levels. L-arginine greately impaired the nicotine-induced hormone responses and reversed the L-NNA elicited enhancement of the nicotine-evoked ACTH and corticosterone response. In contrast to the constitutive eNOS and nNOS antagonists, an inducible NOS antagonist guanethidine (50-100 mg/kg i.p.) did not substantially affect the nicotine-elicited pituitary-adrenocortical responses. Indomethacin (2 mg/kg i.p.), a non-selective cyclooxygenase blocker abolished the L-NAME and L-NNA-induced enhancement of the nicotine-evoked ACTH and corticosterone response. These results indicate that NO is an inhibitory mediator in the HPA axis activity. Inhibition of its generation by eNOS and nNOS significantly enhances the nicotine-induced HPA response. Under basal conditions iNOS is not involved in the nicotine-induced ACTH and corticosterone secretion. Prostaglandins play an obligatory role in the response of HPA axis to systemic nicotine administration.

5

Role of prostaglandins and nitric oxide in the lipopolysaccharide-induced ACTH and corticosterone response

100%

Gadek-Michalska A., Bugajski J.

Journal of Physiology and Pharmacology

|

2004

|

tom 55

|

nr 3

This study was designed to determine the role of endogenous prostaglandins (PG) and nitric oxide (NO) in the lipopolysaccharide (LPS)-induced ACTH and corticosterone secretion in conscious rats. LPS (0.5 and 1 mg/kg) given i.p. stimulated the hypothalamic-pituitary-adrenocortical (HPA) activity measured 2 h later. A non-selective cyclooxygenase inhibitor indomethacin (10 mg/kg i.p.), piroxicam (2 mg/kg i.p.), a more potent antagonist of constitutive cyclooxygenase (COX-1) and compound NS-398 (2 mg/kg i.p.), a selective inhibitor of inducible cyclooxygenase (COX-2) given 30 min before LPS (1 mg/kg i.p.) significantly diminished both the LPS-induced ACTH and corticosterone secretion. COX-2 blocker was the most potent inhibitor of ACTH secretion (72.3%). Nw-nitro-L-arginine methyl ester (L-NAME 2 and 10 mg/kg i.p.), a non-selective nitric oxide synthase (NOS) blocker given 15 min before LPS did not substantially alter plasma ACTH and corticosterone levels 2 h later. Aminoguanidine (AG 100 mg/kg i.p.), a selective inducible nitric oxide synthase (iNOS) inhibitor, considerably enhanced ACTH and corticosterone secretion induced by a lower dose (0.5 mg/kg) of LPS and did not significantly alter this secretion after a larger dose (1 mg/kg) of LPS. L-NAME did not markedly affect the indomethacin-induced inhibition of ACTH and corticosterone response. By contrast, aminoguanidine abolished the indomethacin-induced reduction of ACTH and corticosterone secretion after LPS. These results indicate an opposite action of PG generated by cyclooxygenase and NO synthesized by iNOS in the LPS-induced HPA-response.

6

Physiological mediators in nonsteroidal anti-inflammatory drugs (NSAIDs)-induced impairment of gastric mucosal defense and adaptation. Focus on nitric oxide and lipoxins

100%

Brzozowski T., Konturek P. C., Pajdo R., Ptak-Belowska A., Kwiecien S., Pawlik M., Drozdowicz D., Sliwowski Z., Brzozowski B., Konturek S. J., Pawlik W. W.

Journal of Physiology and Pharmacology. Supplement

|

2008

|

tom 59

|

nr 2

Prostaglandins mediate various physiological aspects of mucosal defense and the suppression of prostaglandin synthesis in the stomach is a critical event in terms of the development of mucosal injury after NSAID administration. However, it has become clear that other mediators besides prostaglandins can similarly act to protect the stomach from injury. For instance, nitric oxide (NO) released from vascular epithelium, epithelial cells of gastrointestinal tract and sensory nerves can influence many of the same components of mucosal defense as do prostaglandins. Thus, administration of NO in a form of NO-donors exert protective influence on the stomach from the injury that usually occurs when mucosal prostaglandin levels are suppressed. The new class of NO releasing NSAIDs, including NO-aspirin, represent a very promising approach to reducing the toxicity of anti-inflammatory drugs. Lipoxins are another group of lipid mediators that can protect the stomach. Aspirin-triggered lipoxin synthesis, via COX-2, acts to reduce the severity of damage induced by this drug. Lipoxin analogues may prove to be useful for preventing mucosal injury and for modulating mucosal inflammation. Aspirin-triggered lipoxin also seems to play in important role in gastric adaptation during chronic aspirin administration. Suppression of COX-2 activity by selective COX-2 inhibitors abolishes the production of this endogenous gastroprotective substance and diminishes the gastric tolerability of NSAIDS and gastric adaptation to these drugs. This review was designed to give an updated overview on the physiological factors and experimental and clinical attempts that were used or may be used in the future as the therapeutic approach to counteract adverse effects in the stomach associated with NSAID ingestion.

7

Involvement of arachidonic acid and its products in the mechanism of progesterone influence on its own production in vitro in bovine corpus luteum

100%

Kotwica J.

Bulletin of the Veterinary Institute in Puławy

|

2004

|

tom 48

|

nr 3

8

Cyclooxygenase pathways

86%

Korbecki J., Baranowska-Bosiacka I., Gutowska I., Chlubek D.

Acta Biochimica Polonica

|

2014

|

tom 61

|

nr 4

9

Prostaglandins of Tetrahymena pyriformis GL-C and T. rostrata

86%

Szablewski L., Hadas E.

Acta Protozoologica

|

1991

|

tom 30

|

nr 3-4

10

The phospholipid contents in rat liver Golgi-rich membrane fractions after streptozotocin and/or prostaglandin treatment

86%

Kordowiak A. M.

Folia Histochemica et Cytobiologica

|

1986

|

tom 24

|

nr 1

11

The influence of inflammatory process on prostaglandin F2alpha contractile activity in porcine uterus

86%

Kucharski J., Jaroszewski J., Jana B., Gorska J., Kozlowska A., Markiewicz W.

Journal of Animal and Feed Sciences

|

2007

|

tom 16

|

nr 4

654-667

12

Resident peritoneal macrophages and mast cells are important cellular sites of COX-1 and COX-2 activity during acute peritoneal inflammation

86%

Kolaczkowska E., Goldys A., Kozakiewicz E., Lelito M., Plytycz B., Van Rooijen N., Arnold B.

Archivum Immunologiae et Therapiae Experimentalis

|

2009

|

tom 57

|

nr 6

459-466

13

Abnormal eicosanoid-pattern of peripheral white-blood-cells in gastro-intestinal cancer

86%

Baenkler H. W., Schafer D.

Journal of Physiology and Pharmacology. Supplement

|

2005

|

tom 56

|

nr 5

119-128

COX-inhibitors promote nasal polyps or bronchial asthma in individuals susceptible to an alteration of the pattern of the eicosanoids, especially leukotrienes and prostaglandins. This is associated with an abnormal release of eicosanoids from white blood cells. Since COX-inhibitors also protect from colorectal cancer an analogous association may be suggested. The study was performed to detect abnormal patterns of eicosanoids in white blood cells of patients with intestinal cancer compared to healthy controls. Seventy patients with intestinal cancer (stomach = 5; colon = 25; sigma = 18; rectum = 22) were compared to 62 healthy controls. Blood leukocytes from patients in complete long-lasting remission were incubated with diluent, arachidonic acid or acetylsalicylic acid. The synthesis of prostaglandin E2 and peptido-leukotrienes was quantified using competitive enzyme-immuno-assays and calculated for individual eicosanoid patterns. The mean basal and arachidonic- or acetylsalicylic acid-modulated PGE2 synthesis in patients was significantly higher than in controls (4.8-fold, 9.4-fold, 3.7-fold, respectively) whereas pLT was generally less elevated. We conclude that the eicosanoid-pattern of white-blood-cells from patients with intestinal cancer differs significantly from that in healthy individuals. This abnormal cellular metabolism may contribute to the manifestation of cancer and help to detect individuals at risk.

14

Psychosocial stress affects the involvement of prostaglandins and nitric oxide in the lipopolysaccharide-induced hypothalamic-pituitary-adrenal response

86%

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

Journal of Physiology and Pharmacology

|

2005

|

tom 56

|

nr 2

The role of prostaglandins and nitric oxide (NO), generated after peripheral lipopolysaccharide (LPS) administration, in the adaptation of hypothalamic-pituitary-adrenal (HPA) axis under stressful circumstances remains to be elucidated. The aim of the present study was to assess the effect of chronic repetitive restraint or social crowding stress on the involvememt of nitric oxide and prostaglandins in the LPS-induced pituitary-adrenocortical response. Male Wistar rats were restrained in metal tubes 2x10 min/day or crowded in cages for 7 days prior to treatment. All compounds were injected i.p., cyclooxygenase (COX) and nitric oxide synthase (NOS) inhibitors 15 min before LPS. Two hrs after injection LPS induced a significant increase in ACTH and corticosterone secretion. Repeated restraint impaired more potently than crowding stress the LPS-induced HPA-response. Indomethacin, a non-selective COX inhibitor, considerably reduced the LPS-induced HPA response in non-stressed rats and to a lesser extent diminished this response in repeatedly restrained or crowded rats. Neuronal NOS inhibitor, Nw-nitro-L-arginine decreased the LPS-induced HPA response, more potently in control than crowded rats. Aminoguanidine, an iNOS inhibitor, diminished the LPS-elicited ACTH response in crowded rats. These results indicate that prostaglandins and NO generated by neuronal and inducible NOS are involved in the LPS-induced HPA axis response under basal conditions and during its adaptation to chronic social stress circumstances.

15

GnRH-PGF 2a and PGF 2a-PGF 2a synchronization in Akkaraman cross-bred sheep in the breeding season

86%

Rozkurt Ataman M., Akoz M.

Bulletin of the Veterinary Institute in Puławy

|

2006

|

tom 50

|

nr 1

16

The effect of danazol on the activity of peritoneal macrophages

86%

Kurzawa R., Barcew-Wiszniewska B., Skowron J.

Folia Histochemica et Cytobiologica

|

1997

|

tom 35

|

nr 2

17

Effect and mechanism of sucralfate on healing of acetic acid-induced gastric ulcers in rats

86%

Ogihara Y., Okabe S.

Journal of Physiology and Pharmacology

|

1993

|

tom 44

|

nr 2

18

Ghrelin - a new gastroprotective factor in gastric mucosa

86%

Konturek P. C., Brzozowski T., Pajdo R., Nikiforuk A., Kwiecien S., Harsch I., Drozdowicz D., Hahn E. G., Konturek S. J.

Journal of Physiology and Pharmacology

|

2004

|

tom 55

|

nr 2

Ghrelin, a novel peptide expressed in the gastrointestinal tract, especially in the gastric mucosa, exerts several biological activities including the stimulation of appetite and food intake, the stimulation of intestinal motility and the release of growth hormone. The aim of this study was to examine the expression of ghrelin in gastric mucosa after its exposure to ethanol and its effects on gastric lesions induced by ethanol with and without pretreatment with indomethacin. Acute gastric lesions were induced by intragastric administration of 75% ethanol in rats pretreated with saline-vehicle or ghrelin injected intraperitoneally (i.p.) without or with i.p. pretreatment with indomethacin. At the end of experiments, the rats were anesthetized, the stomach was exposed to measure gastric blood flow (GBF), to determine the area of gastric lesions and to take biopsy samples from the oxyntic mucosa for determination of transcripts of ghrelin, tumor necrosis alpha (TNF-alpha) and transforming growth factor alpha (TGFalpha) using RT-PCR and to assess the generation of PGE2 by RIA. Exposure of gastric mucosa to 75% ethanol resulted in numerous mucosal lesions of an area of about 115 mm2 and in the increase of mucosal expression of TNF-alpha, PGE2, TGFalpha and ghrelin with concomitant decrease in GBF. Exogenous ghrelin reduced dose-dependently acute gastric lesions with simultaneous attenuation of GBF and a decrease in the expression of TNF-alpha but not TGFalpha. Pretreatment with indometahcin, which suppressed the generation of PGE2 by about 85%, augmented ethanol-induced gastric lesions and eliminated the ghrelin-induced protection of mucosa against ethanol. We conclude that ghrelin, whose mucosal expression is enhanced after exposure to ethanol, exhibits a strong gastroprotection, at least in part, due to its anti-inflammatory action mediated by prostaglandins.

19

Effects of prostaglandins on [Ca2] and adenylate cyclase activity in isolated porcine gastric mucous cells

86%

Heim H. K., Bersimbaev R. I., Gandjour A., Beil W., Sewing K. F.

Journal of Physiology and Pharmacology

|

1994

|

tom 45

|

nr 2

20

Inhibition of cyclooxygenase-2 by diallyl sulfides [DAS] in HEK 293T cells

86%

Elango E. M., Asita H., Nidhi G., Seema P., Banerji A., Kuriakose M. A.

Journal of Applied Genetics

|

2004

|

tom 45

|

nr 4

Ograniczanie wyników