Wyniki wyszukiwania

1

Synthesis of L-cysteine derivatives of immunotropic activity

100%

Kwapiszewski W., Sokolowska-Muszynska M., Iliaszenko J., Borkowski L., Witczak M.

Archivum Immunologiae et Therapiae Experimentalis

|

1989

|

tom 37

|

nr 1-2

2

Antileukotriene treatment and allergic rhinitis-related cough in guinea pigs

72%

Brozmanova M., Plevkova J., Bartos V., Plank L., Tatar M.

Journal of Physiology and Pharmacology. Supplement

|

2005

|

tom 56

|

nr 4

21-30

Experimental allergic rhinitis produces enhanced cough response in awake guinea pigs. Leukotriene receptor antagonists, as anti-inflammatory agents, have been effective in treatment of asthma and allergic rhinitis to inhibit the early and late allergic response. In the present study, we evaluated the effect of montelukast (Singulair, Merck, USA) on the cough reflex in an experimental model of allergen-induced rhinitis in guinea pigs. Guinea pigs (n=16) were sensitized with intraperitoneal ovalbumin (OVA). The animals were then used to develop a model of allergic rhinitis by repeated intranasal instillation of 0.5% OVA at weekly intervals for 8 weeks. Allergic rhinitis was evaluated from the occurrence of typical clinical symptoms including sneezing, conjuctival and nasal secretion, or nasal acoustic phenomenon. Between the 6th and 8th nasal challenge (NCh) the animals (n=8) were treated daily for 14 days with oral montelukast (10mg/kg). Cough was induced by citric acid aerosol inhalation in gradually increasing concentration (0.05-1.6 M) and was evaluated before sensitization and then after the 1st, 6th, and 8th nasal challenge when rhinitic symptoms were most conspicuous. The intensity of cough was significantly increased after the first and repeated nasal OVA challenges, and reduced after the 8th NCh that was preceded with montelukast treatment [9(6-14) vs. 16.5(14-22) vs. 25.5(23-42) vs. 8.5(8-13); P=0.0003]. We conclude that antileukotriene therapy suppresses the stimulating effect of experimental allergic rhinitis on the chemically-induced cough in awake guinea pigs.

3

Matrix metalloproteinases activity during the evolution of hypoxic-ischemic brain damage in the immature rat. The effect of 1-methylnicotinamide (MNA)

72%

Dragun P., Makarewicz D., Wojcik L., Ziemka-Nalecz M., Slomka M., Zalewska T.

Journal of Physiology and Pharmacology

|

2008

|

tom 59

|

nr 3

441-455

Matrix metalloproteinases (MMPs) are a family of proteolytic enzymes that degrade the extracellular matrix and carry out key functions during brain development. Apart from a physiological role, excessive activation of MMPs in brain tissue has been postulated to represent a pathway for cell death arising from ischemia. To evaluate the possible involvement of MMPs in the perinatal brain asphyxia, we exposed 7-day-old rats to hypoxia-ischemia (HI). Unilateral HI was administered by ligation of the common carotid artery followed by hypoxia (7.4% O2/92.6% N2) for 65 minutes. This insult is known to produce brain damage confined to the cerebral hemisphere ipsilateral to the arterial occlusion in > 90% of animals. HI resulted in a significant elevation of MMP-2 and MMP-9 activity in the ipsilateral forebrain. The maximum activation was found at 48 hours and 7-14 days after the insult. These results suggest that early and late induction of MMPs may play a role in neuronal death as well as in repair processes. The treatment of animals subjected to HI with 1-methylnicotinamide (MNA), the anti-inflammatory agent, led to the inhibition of MMP-9 in an acute phase of ischemic damage and to the activation of MMP-2 in the later stages after injury. The timing of MMPs modulation by MNA may indicate its possible therapeutic implications.

4

Inter-alpha-inhibitor, hyaluronan and inflammation

72%

Fries E., Kaczmarczyk A.

Acta Biochimica Polonica

|

2003

|

tom 50

|

nr 3

Inter-a-inhibitor is an abundant plasma protein whose physiological function is only now beginning to be revealed. It consists of three polypeptides: two heavy chains and one light chain called bikunin. Bikunin, which has antiproteolytic activity, carries a chondroitin sulphate chain to which the heavy chains are covalently linked. The heavy chains can be transferred from inter-a-inhibitor to hyaluronan molecules and become covalently linked. This reaction seems to be mediated by TSG-6, a protein secreted by various cells upon stimulation by inflammatory cytokines. Inter-a-inhibitor has been shown to be required for the stabilization of the cumulus cell-oocyte complex during the expansion that occurs prior to ovulation. Hyaluronan-linked heavy chains in the extracellular matrix of this cellular complex have recently been shown to be tightly bound to TSG-6. Since TSG-6 binds to hyaluronan, its complex with heavy chains could stabilize the extracellular matrix by cross-linking hyaluronan molecules. Heavy chains linked to hyaluronan molecules have also been found in inflamed tissues. The physiological role of these complexes is not known but there are indications that they might protect hyaluronan against fragmentation by reactive oxygen species. TSG-6 also binds to bikunin thereby enhancing its antiplasmin activity. Taken together, these results suggest that inter-a-inhibitor is an anti-inflammatory agent which is activated by TSG-6.

5

1-methylnicotinamide and nicotinamide: two related anti-inflammatory agents that differentially affect the functions of activated macrophages

72%

Biedron R., Ciszek M., Tokarczyk M., Bobek M., Kurnyta M., Slominska E. M., Smolenski R. T., Marcinkiewicz J.

Archivum Immunologiae et Therapiae Experimentalis

|

2008

|

tom 56

|

nr 2

6

Pneumolysins as a vaccine and drug target in the prevention and treatment of invasive pneumococcal disease

72%

Cockeran R., Anderson R., Feldman C.

Archivum Immunologiae et Therapiae Experimentalis

|

2005

|

tom 53

|

nr 3

7

The analgesic and anticonvulsant effects of piperine in mice

58%

Bukhari I. A., Alhumayyd M. S., Mahesar A. L., Gilani A. H.

Journal of Physiology and Pharmacology

|

2013

|

tom 64

|

nr 6

8

15-deoxy-delta12,14-prostaglandin J2 suppresses RANTES expression by inhibiting NADPH oxidase activation in Helicobater pylori-infected gastric epithelial cells

58%

Cha B., Lim J. W., Kim K. H., Kim H.

Journal of Physiology and Pharmacology

|

2011

|

tom 62

|

nr 2

Peroxisome proliferators-activated receptor-g (PPAR-g) is a ligand-activated transcription factor. 15 deoxy-12,14 prostaglandin J2 (15d-PGJ2) is a potent PPAR- ligand and acts as an anti-inflammatory agent via PPAR--dependent and independent mechanisms. Helicobacter pylori (H. pylori) induces gastric inflammation by inducing the activation of oxidant-sensitive transcription factor NF-B and cytokine expression in gastric epithelial cells. Since 15d-PGJ2 inhibits NF-B activation in various cells, it may suppress H. pylori-induced inflammatory signaling and cytokine expression in gastric epithelial cells. The present study aims to determined the effect of 15d-PGJ2 on the activation of inflammatory mediators Jak/Stat (Janus kinase/signal transducers and activators of transcription) and induction of cytokine RANTES in H. pylori-infected gastric epithelial AGS cells. Since NADPH oxidase is a candidate for the production of reactive oxygen species in H. pylori-infected gastric epithelial cells, we determined the effect of 15d-PGJ2 on the activation of NADPH oxdase. AGS cells were cultured in the presence of H. pylori treated with or without 15d-PGJ2. The activations of NADPH oxidase and Jak1/Stat3, the levels of H2O2 and RANTES in the medium, and DNA binding activity of Stat3 were assessed. A Jak/Stat3 specific inhibitor AG490 and an inhibitor of NADPH oxidase diphenyleneiodonium (DPI) were treated to determine the direct involvement of Jak/Stat and NADPH oxidase on the production of H2O2 and RANTES in H. pylori-infected cells. H. pylori induced the production of H2O2 and RANTES as well as the activations of NADPH oxidase and Jak1/Stat3, which were inhibited by the treatment of 15d-PGJ2. DPI suppressed H. pylori-induced alterations similar to 15d-PGJ2. However, AG490 had no effect on NADPH oxidase activation, but reduced the level of RANTES in the medium released from H. pylori-infected cells. Conclusion: NADPH oxidase activation is an upstream signaling of Jak1/Stat3 activation and induction of RANTES in H. pylori-infected AGS cells. 15d-PGJ2, inhibits the activations of NADPH oxidase and Jak1/Stat3 and RANTES expression, suggesting that 15d-PGJ2 may be beneficial for the treatment of H. pylori-induced gastric inflammation.

Ograniczanie wyników

Synthesis of L-cysteine derivatives of immunotropic activity

Antileukotriene treatment and allergic rhinitis-related cough in guinea pigs

Matrix metalloproteinases activity during the evolution of hypoxic-ischemic brain damage in the immature rat. The effect of 1-methylnicotinamide (MNA)

Inter-alpha-inhibitor, hyaluronan and inflammation

1-methylnicotinamide and nicotinamide: two related anti-inflammatory agents that differentially affect the functions of activated macrophages

Pneumolysins as a vaccine and drug target in the prevention and treatment of invasive pneumococcal disease

The analgesic and anticonvulsant effects of piperine in mice

15-deoxy-delta12,14-prostaglandin J2 suppresses RANTES expression by inhibiting NADPH oxidase activation in Helicobater pylori-infected gastric epithelial cells