ncr-631 and Anorexia

ncr-631 has been researched along with Anorexia* in 1 studies

Other Studies

1 other study(ies) available for ncr-631 and Anorexia

Article	Year
Effects of the 3-hydroxyanthranilic acid analogue NCR-631 on anoxia-, IL-1 beta- and LPS-induced hippocampal pyramidal cell loss in vitro. Amino acids, 1998, Volume: 14, Issue:1-3 The kynurenine pathway intermediate 3-hydroxyanthranilic acid (3-HANA) is converted by 3-HANA 3,4-dioxygenase (3-HAO) to the putative neuropathogen quinolinic acid (QUIN). In the present study, the neuroprotective effects of the 3-HANA analogue and 3-HAO inhibitor NCR-631 was investigated using organotypic cultures of rat hippocampus. An anoxic lesion was induced by exposing the cultures to 100% N2 for 150 min, resulting in a pronounced loss of pyramidal neurons, as identified using NMDA-R1 receptor subunit immunohistochemistry. NCR-631 provided a concentration-dependent protective effect against the anoxia. NCR-631 was also found to counteract the loss of pyramidal neurons in two models of neuroinflammatory-related damage; incubation with either LPS (10 ng/ml) or IL-1 beta (10 IU/ml). The findings suggest that NCR-631 has neuroprotective properties and that it may be a useful tool to study the role of kynurenines in neurodegeneration. Topics: 3-Hydroxyanthranilic Acid; Animals; Anorexia; Disease Models, Animal; Hippocampus; Immunohistochemistry; Interleukin-1; Lipopolysaccharides; N-Methylaspartate; Organ Culture Techniques; Pyramidal Cells; Rats; Rats, Sprague-Dawley	1998

Article

Year

Effects of the 3-hydroxyanthranilic acid analogue NCR-631 on anoxia-, IL-1 beta- and LPS-induced hippocampal pyramidal cell loss in vitro.

Amino acids, 1998, Volume: 14, Issue:1-3

The kynurenine pathway intermediate 3-hydroxyanthranilic acid (3-HANA) is converted by 3-HANA 3,4-dioxygenase (3-HAO) to the putative neuropathogen quinolinic acid (QUIN). In the present study, the neuroprotective effects of the 3-HANA analogue and 3-HAO inhibitor NCR-631 was investigated using organotypic cultures of rat hippocampus. An anoxic lesion was induced by exposing the cultures to 100% N2 for 150 min, resulting in a pronounced loss of pyramidal neurons, as identified using NMDA-R1 receptor subunit immunohistochemistry. NCR-631 provided a concentration-dependent protective effect against the anoxia. NCR-631 was also found to counteract the loss of pyramidal neurons in two models of neuroinflammatory-related damage; incubation with either LPS (10 ng/ml) or IL-1 beta (10 IU/ml). The findings suggest that NCR-631 has neuroprotective properties and that it may be a useful tool to study the role of kynurenines in neurodegeneration.

Topics: 3-Hydroxyanthranilic Acid; Animals; Anorexia; Disease Models, Animal; Hippocampus; Immunohistochemistry; Interleukin-1; Lipopolysaccharides; N-Methylaspartate; Organ Culture Techniques; Pyramidal Cells; Rats; Rats, Sprague-Dawley

1998