carbocyanines and Asphyxia-Neonatorum

carbocyanines has been researched along with Asphyxia-Neonatorum* in 1 studies

Other Studies

1 other study(ies) available for carbocyanines and Asphyxia-Neonatorum

Article	Year
Allopregnanolone attenuates N-methyl-D-aspartate-induced excitotoxicity and apoptosis in the human NT2 cell line in culture. Neuroscience letters, 2002, Aug-02, Volume: 328, Issue:1 Progesterone modulates gamma-aminobutyric acid and excitatory amino acid neurotransmitter systems and has neuroprotective properties in models of hypoxia-ischemia. This study examined the in vitro effects of allopregnanolone, the active progesterone metabolite, in models of N-methyl-D-aspartate (NMDA)-induced necrosis and apoptosis. Cultured NT2 neurons were exposed to 1 mM NMDA. Lactate dehydrogenase (LDH) release was measured 24 h later. NMDA at a concentration of 1 mM produced a 39 +/- 19% release of total LDH. Exposure to 10 microM allopregnanolone prior to NMDA exposure reduced LDH release by 51% (P = 0.0028). NMDA stimulated apoptotic cell changes defined by terminal dUTP nick-end labeling (TUNEL) and 5,5', 6,6'-tetrachloro-1,1,3,3'-tetra ethlybenzimidazolycarbocyanide iodide staining were reduced to baseline values by both 10 microM allopregnanolone and 100 microM MK-801. Pretreatment with allopregnanolone (0-10 microM) reduced the percentage of TUNEL-positive cells in a dose-dependent manner (EC(50) = 2.7 +/- 0.1 nM). Physiologic concentrations of allopregnanolone provided protection against both necrotic and apoptotic injury induced by NMDA excitotoxicity. Topics: Apoptosis; Asphyxia Neonatorum; Benzimidazoles; Carbocyanines; Cell Count; Cell Survival; Dizocilpine Maleate; Dose-Response Relationship, Drug; Excitatory Amino Acid Agonists; Excitatory Amino Acid Antagonists; Female; Fluorescent Dyes; Humans; Hypoxia-Ischemia, Brain; In Situ Nick-End Labeling; Infant, Newborn; L-Lactate Dehydrogenase; Membrane Potentials; Mitochondria; N-Methylaspartate; Neurons; Neuroprotective Agents; Neurotoxins; Pregnancy; Pregnanolone; Progesterone; Tumor Cells, Cultured	2002

Article

Year

Allopregnanolone attenuates N-methyl-D-aspartate-induced excitotoxicity and apoptosis in the human NT2 cell line in culture.

Neuroscience letters, 2002, Aug-02, Volume: 328, Issue:1

Progesterone modulates gamma-aminobutyric acid and excitatory amino acid neurotransmitter systems and has neuroprotective properties in models of hypoxia-ischemia. This study examined the in vitro effects of allopregnanolone, the active progesterone metabolite, in models of N-methyl-D-aspartate (NMDA)-induced necrosis and apoptosis. Cultured NT2 neurons were exposed to 1 mM NMDA. Lactate dehydrogenase (LDH) release was measured 24 h later. NMDA at a concentration of 1 mM produced a 39 +/- 19% release of total LDH. Exposure to 10 microM allopregnanolone prior to NMDA exposure reduced LDH release by 51% (P = 0.0028). NMDA stimulated apoptotic cell changes defined by terminal dUTP nick-end labeling (TUNEL) and 5,5', 6,6'-tetrachloro-1,1,3,3'-tetra ethlybenzimidazolycarbocyanide iodide staining were reduced to baseline values by both 10 microM allopregnanolone and 100 microM MK-801. Pretreatment with allopregnanolone (0-10 microM) reduced the percentage of TUNEL-positive cells in a dose-dependent manner (EC(50) = 2.7 +/- 0.1 nM). Physiologic concentrations of allopregnanolone provided protection against both necrotic and apoptotic injury induced by NMDA excitotoxicity.

Topics: Apoptosis; Asphyxia Neonatorum; Benzimidazoles; Carbocyanines; Cell Count; Cell Survival; Dizocilpine Maleate; Dose-Response Relationship, Drug; Excitatory Amino Acid Agonists; Excitatory Amino Acid Antagonists; Female; Fluorescent Dyes; Humans; Hypoxia-Ischemia, Brain; In Situ Nick-End Labeling; Infant, Newborn; L-Lactate Dehydrogenase; Membrane Potentials; Mitochondria; N-Methylaspartate; Neurons; Neuroprotective Agents; Neurotoxins; Pregnancy; Pregnanolone; Progesterone; Tumor Cells, Cultured

2002