biie-0246 and Endotoxemia

biie-0246 has been researched along with Endotoxemia* in 1 studies

Other Studies

1 other study(ies) available for biie-0246 and Endotoxemia

Article	Year
Distinct effects of NPY13-36, a specific NPY Y2 agonist, in a model of rodent endotoxemia on leukocyte subsets and cytokine levels. Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft, 2011, Dec-20, Volume: 193, Issue:6 Even now, sepsis remains a major problem in modern clinical medicine, leading to systemic inflammatory response including altered leukocyte subset distribution and increased cytokine release. As immune cells are known to express NPY receptors, we investigated the effects of a specific NPY Y(2) receptor agonist (NPY(13-36)) and/or the corresponding Y(2) receptor antagonist BIIE0246 treatment on blood (by FACS analyses) and tissue (by immunohistochemistry) leukocyte subsets as well as on levels of IL-4, IL-6, IL-10, TNF-α, INF-γ (by Cytometric Bead Array) in healthy and acutely endotoxemic rats. Results show a significant decrease in blood monocytes after LPS challenge in endotoxemic control animals (by 93%), in endotoxemic NPY(13-36) treated animals (by 83%) and in endotoxemic BIIE0246 treated animals (by 88%) as compared to the corresponding healthy controls. Endotoxemic control animals showed a significant increase of TNF-α (by 98%) as compared to the healthy control group. A treatment with NPY(13-36) significantly stabilized TNF-α level in endotoxemic animals. This study indicates distinct subset- and cytokine-specific in vivo effects induced by an NPY Y(2) receptor specific treatment after a short-term LPS challenge. Topics: Animals; Arginine; Benzazepines; Cells, Cultured; Cytokines; Endotoxemia; Leukocytes; Male; Neuropeptide Y; Peptide Fragments; Rats; Rats, Inbred Lew; Receptors, Neuropeptide Y	2011

Article

Year

Distinct effects of NPY13-36, a specific NPY Y2 agonist, in a model of rodent endotoxemia on leukocyte subsets and cytokine levels.

Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft, 2011, Dec-20, Volume: 193, Issue:6

Even now, sepsis remains a major problem in modern clinical medicine, leading to systemic inflammatory response including altered leukocyte subset distribution and increased cytokine release. As immune cells are known to express NPY receptors, we investigated the effects of a specific NPY Y(2) receptor agonist (NPY(13-36)) and/or the corresponding Y(2) receptor antagonist BIIE0246 treatment on blood (by FACS analyses) and tissue (by immunohistochemistry) leukocyte subsets as well as on levels of IL-4, IL-6, IL-10, TNF-α, INF-γ (by Cytometric Bead Array) in healthy and acutely endotoxemic rats. Results show a significant decrease in blood monocytes after LPS challenge in endotoxemic control animals (by 93%), in endotoxemic NPY(13-36) treated animals (by 83%) and in endotoxemic BIIE0246 treated animals (by 88%) as compared to the corresponding healthy controls. Endotoxemic control animals showed a significant increase of TNF-α (by 98%) as compared to the healthy control group. A treatment with NPY(13-36) significantly stabilized TNF-α level in endotoxemic animals. This study indicates distinct subset- and cytokine-specific in vivo effects induced by an NPY Y(2) receptor specific treatment after a short-term LPS challenge.

Topics: Animals; Arginine; Benzazepines; Cells, Cultured; Cytokines; Endotoxemia; Leukocytes; Male; Neuropeptide Y; Peptide Fragments; Rats; Rats, Inbred Lew; Receptors, Neuropeptide Y

2011