Wyniki wyszukiwania

1

Effect of pentoxifylline on the development of apoptosis-like changes in experimental lung damage

100%

Sulkowska M., Sulkowski S.

Folia Histochemica et Cytobiologica

|

1999

|

tom 37

|

nr 2

2

Stress-induced rise in endothelaemia, von Willebrand factor and hypothalamic-pituitary-adrenocortical axis activation is reduced by pretreatment with pentoxifylline

84%

Jezova D., Kristova V., Slamova J., Mlynarik M., Pirnik Z., Kiss A., Kriska M.

Journal of Physiology and Pharmacology

|

2003

|

tom 54

|

nr 3

Stress is considered to be a risk factor of several diseases. The following hypotheses were tested: (1) single exposure to an intensive stressor is followed by endothelial stimulation and/or damage to endothelial cells, (2) potential stress-induced endothelial cell damage is reduced by repeated pretreatment with pentoxifylline and (3) pentoxifylline treatment modifies neuroendocrine activation during stress reflected by changes in hypothalamic-pituitary-adrenocortical (HPA) axis function. Rats were treated with saline or pentoxifylline (20 mg/kg, s.c.) once daily for 7 days and then exposed to single immobilization stress for 20 or 120 min. In saline pretreated rats, stress exposure was followed by a rise in endothelaemia, von Willebrand factor concentrations, adrenocorticotropic hormone (ACTH) and corticosterone release, as well as by enhanced gene expression of hypothalamic corticotropin releasing factor (CRH). Stress-induced changes were reduced by pretreatment with pentoxifylline. Significant inhibition was observed in endothelaemia, plasma ACTH and corticosterone concentration in the adrenals. Thus, signs of endothelial injury as well as stress-induced hormone levels were reduced by pretreatment with pentoxifylline, although there is no evidence for a causal relationship. This protective action of pentoxifylline might be of benefit in the prevention and therapy of some stress-related disorders.

3

Methylxanthines [caffeine, pentoxifylline and theophylline] decrease the mutagenic effect of daunomycin, doxorubicin and mitoxantrone

84%

Piosik J., Gwizdek-Wisniewska A., Ulanowska K., Ochocinski J., Czyz A., Wegrzyn G.

Acta Biochimica Polonica

|

2005

|

tom 52

|

nr 4

Previously performed experiments showed that methylxanthines, especially caffeine, may protect cells against cytostatic or cytotoxic effects of several aromatic compounds. One of the proposed mechanisms of this protection is based on stacking interactions between π electron systems of polycyclic aromatic molecules. In this work, we demonstrate that caffeine and other methylxanthines - pentoxifylline and theophylline - significantly decrease mutagenicity of the anticancer aromatic drugs daunomycin, doxorubicin and mitoxantrone. The spectrophotometric titration of these aromatic compounds by methylxanthines indicated formation of mixed aggregates. The concentrations of free active forms of the drugs decreased when the concentrations of methylxanthines increased in the mixture. Therefore, likely methylxanthines may play a role of scavengers of the free active forms of daunomycin, doxorubicin and mitoxantrone.

4

Mechanism of action of the sperm motility inhibiting factor [SMIF] from boar seminal plasma

84%

Kordan W.

Natural Sciences

|

1999

|

tom 02

5

Effect of pentoxifylline on biochemical parameters in endotoxaemic New Zealand white rabbits

84%

Yazar E., Col R., Uney K., Atalay B., Elmas M., Tras B.

Bulletin of the Veterinary Institute in Puławy

|

2004

|

tom 48

|

nr 3

6

Modulation of inflammatory response by pentoxifylline is independent of heme oxygenase-1 pathway

67%

Taha H., Grochot-Przeczek A., Was H., Kotlinowski J., Kozakowska M., Marek A., Skrzypek K., Lackowska B., Balcerczyk A., Mustafa S., Dulak J., Jozkowicz A.

Journal of Physiology and Pharmacology

|

2009

|

tom 60

|

nr 2

3-12

Objective: It was reported that some effects of pentoxifylline (PTX) are mediated by heme oxygenase-1 (HO-1) induction. We investigated the role of HO-1 in anti-inflammatory activity of PTX. Methods: Experiments were performed in human and murine monocytes and endothelial cells and in HO-1 deficient mice. Results: PTX dose-dependently decreased expression of HO-1 in cell lines studied. As expected, PTX reduced also production of TNF. This effect was independent of HO-1 activity, as demonstrated in cells treated with HO-1 activators and inhibitors or in cells overexpressing HO-1. Moreover, inhibition of TNF was the same in human endothelial cells of different HO-1 genotypes, showing that PTX is similarly efficient in carriers of more and less active HO-1 promoter variants. In mice, PTX did not influence HO-1 expression, as measured in liver, kidney, spleen, heart, and skin. Accordingly, the response of PTX treated animals to LPS was the same in wild type and HO-1 deficient mice. PTX to a similar extent increased influx of leukocyte into peritoneal cavity, decreased production of TNF and reduced expression of VCAM-1 in vascular intima. Conclusion: PTX inhibits production of TNF and may decrease inflammatory reaction both in vitro and in vivo, but these effects are independent of HO-1.

7

Alveolar cells in cyclophosphamide-induced lung injury. The effect of pentoxifylline on BAL-isolated cells

67%

Sulkowska M., Sulkowski S.

Folia Histochemica et Cytobiologica

|

1998

|

tom 36

|

nr 2

Ograniczanie wyników

Effect of pentoxifylline on the development of apoptosis-like changes in experimental lung damage

Stress-induced rise in endothelaemia, von Willebrand factor and hypothalamic-pituitary-adrenocortical axis activation is reduced by pretreatment with pentoxifylline

Methylxanthines [caffeine, pentoxifylline and theophylline] decrease the mutagenic effect of daunomycin, doxorubicin and mitoxantrone

Mechanism of action of the sperm motility inhibiting factor [SMIF] from boar seminal plasma

Effect of pentoxifylline on biochemical parameters in endotoxaemic New Zealand white rabbits

Modulation of inflammatory response by pentoxifylline is independent of heme oxygenase-1 pathway

Alveolar cells in cyclophosphamide-induced lung injury. The effect of pentoxifylline on BAL-isolated cells