1-Methylnicotinamide attenuates lipopolysaccharide-induced cognitive deficits via targeting neuroinflammation and neuronal apoptosis - Mu, Rong-hao; Tan, Yuan-zhi; Fu, Li-li; Nazmul Islam, Mohammad; Hu, Mei; Hong, Hao; Tang, Su-su (International immunopharmacology, 2019)
Keywords: 1-Methylnicotinamide; Alzheimer's disease; Animals; Anti-Inflammatory Agents - pharmacology; Anti-Inflammatory Agents - therapeutic use; Apoptosis; Apoptosis - drug effects; Astrocytes; BAX protein; Bcl-2 protein; Caspase-3; Cell activation; Cognition; Cognition deficits; Cognition Disorders - chemically induced; Cognition Disorders - drug therapy; Cognition Disorders - immunology; Cognitive ability; Cortex (frontal); Cytokines; Frontal Lobe - drug effects; Hippocampus; Hippocampus - drug effects; Inflammation; Interleukin 6; Interleukin-6 - immunology; Lipopolysaccharide; Lipopolysaccharides; Male; Memory Disorders - chemically induced; Memory Disorders - drug therapy; Memory Disorders - immunology; Metabolites; Mice, Inbred ICR; Microglia; Neurodegenerative diseases; Neuroinflammation; Neuronal apoptosis; Neurons - drug effects; Neuroprotection; Neuroprotective Agents - pharmacology; Neuroprotective Agents - therapeutic use; NF-κB protein; Niacinamide - analogs & derivatives; Niacinamide - pharmacology; Niacinamide - therapeutic use; Nicotinamide; Object recognition; Pattern recognition; Transcription Factor RelA - immunology; Tumor Necrosis Factor-alpha - immunology; Tumor necrosis factor-α; Lipopolysaccharide; Cognition deficits; Neuroinflammation; Neuronal apoptosis; 1-Methylnicotinamide