u-0126 and 7-7-dimethyl-5-8-eicosadienoic-acid

u-0126 has been researched along with 7-7-dimethyl-5-8-eicosadienoic-acid* in 1 studies

Other Studies

1 other study(ies) available for u-0126 and 7-7-dimethyl-5-8-eicosadienoic-acid

Article	Year
Discussion of the role of the extracellular signal-regulated kinase-phospholipase A2 pathway in production of reactive oxygen species in Alzheimer's disease. Neurochemical research, 2003, Volume: 28, Issue:2 In this paper we show that exposure of a rat brain synaptosome fraction to the amyloid beta peptide fragment betaA(25-35), but not the inverted peptide betaA(35-25), stimulated production of reactive oxygen species (ROS) in a concentration- and time-dependent manner. The ROS formation was attenuated by the tyrosine kinase inhibitor genistein, the mitogen-activated protein kinase inhibitor U0126, and the phospholipase A2 (PLA2) inhibitor 7,7-dimethyl-(5Z,8Z)-eicosadienoic acid. This strongly suggests that betaA(25-35) stimulated ROS production through an extracellular signal-regulated kinase-PLA2-dependent pathway. The interaction between these enzymes and their possible involvement in free radical formation in Alzheimer's disease are discussed. Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Brain; Butadienes; Enzyme Inhibitors; Fatty Acids, Unsaturated; Genistein; Mitogen-Activated Protein Kinase 1; Mitogen-Activated Protein Kinase 3; Mitogen-Activated Protein Kinases; Nitriles; Peptide Fragments; Phospholipases A; Phospholipases A2; Rats; Reactive Oxygen Species; Spectrometry, Fluorescence; Synaptosomes	2003

Article

Year

Discussion of the role of the extracellular signal-regulated kinase-phospholipase A2 pathway in production of reactive oxygen species in Alzheimer's disease.

Neurochemical research, 2003, Volume: 28, Issue:2

In this paper we show that exposure of a rat brain synaptosome fraction to the amyloid beta peptide fragment betaA(25-35), but not the inverted peptide betaA(35-25), stimulated production of reactive oxygen species (ROS) in a concentration- and time-dependent manner. The ROS formation was attenuated by the tyrosine kinase inhibitor genistein, the mitogen-activated protein kinase inhibitor U0126, and the phospholipase A2 (PLA2) inhibitor 7,7-dimethyl-(5Z,8Z)-eicosadienoic acid. This strongly suggests that betaA(25-35) stimulated ROS production through an extracellular signal-regulated kinase-PLA2-dependent pathway. The interaction between these enzymes and their possible involvement in free radical formation in Alzheimer's disease are discussed.

Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Brain; Butadienes; Enzyme Inhibitors; Fatty Acids, Unsaturated; Genistein; Mitogen-Activated Protein Kinase 1; Mitogen-Activated Protein Kinase 3; Mitogen-Activated Protein Kinases; Nitriles; Peptide Fragments; Phospholipases A; Phospholipases A2; Rats; Reactive Oxygen Species; Spectrometry, Fluorescence; Synaptosomes

2003