title: Mechanism of soluble beta-amyloid 25-35 neurotoxicity in primary cultured rat cortical neurons.
abstract: This study aimed to determine the effects of different concentrations of soluble beta-amyloid 25-35 (Aβ25-35) on cell viability, calcium overload, and PI3K-p85 expression in cultured cortical rat neurons. Primary cultured cerebral cortical neurons of newborn rats were divided randomly into six groups. Five groups were treated with soluble Aβ25-35 at concentrations of 10nmol/L, 100nmol/L, 1μmol/L, 10μmol/L, or 30μmol/L. Cell Counting Kit-8 staining was used to measure cell viability, laser-scanning confocal imaging was used to detect changes in intracellular free calcium concentration, and western blot assay was used to measure neuronal PI3K-p85 expression. Soluble Aβ25-35 was found to reduce cell viability and induce calcium overload in primary cultured rat cerebral cortical neurons, in a concentration-dependent manner. At certain concentrations, soluble Aβ25-35 also increased neuronal PI3K-p85 expression. These findings reveal that soluble Aβ25-35 reduces the viability of cultured cerebral cortical rat neurons. The neurotoxicity mechanism may involve calcium overload and disruption of insulin signal transduction pathways.
authors.affiliation: Department of Pain Medicine, Aviation General Hospital of China Medical University & Beijing Institute of Translational Medicine, Chinese Academy of Sciences, Beijing 100012, China.
authors.forename: Yong
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Neurology, Second Hospital of Shanxi Medical University, Taiyuan 030001, Shanxi, China.
authors.forename: Lili
authors.initials: L
authors.lastname: Liu
authors.affiliation: Department of Neurology, Second Hospital of Shanxi Medical University, Taiyuan 030001, Shanxi, China. Electronic address: HuWeimin201409@163.com.
authors.forename: Weimin
authors.initials: W
authors.lastname: Hu
authors.affiliation: Department of Neurology, Second Hospital of Shanxi Medical University, Taiyuan 030001, Shanxi, China.
authors.forename: Guanglai
authors.initials: G
authors.lastname: Li
mesh_terms: D016229:Amyloid beta-Peptides / Q000378:metabolism* / Q000633:toxicity; D000818:Animals; D000831:Animals, Newborn; D002118:Calcium / Q000378:metabolism; D002470:Cell Survival; D002540:Cerebral Cortex / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D058543:Class Ia Phosphatidylinositol 3-Kinase / Q000378:metabolism; D007328:Insulin / Q000502:physiology; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D010446:Peptide Fragments / Q000378:metabolism* / Q000633:toxicity; D061251:Primary Cell Culture; D017208:Rats, Wistar; D015398:Signal Transduction; D012995:Solubility
chemical_list: D016229:Amyloid beta-Peptides; D007328:Insulin; D010446:Peptide Fragments; C074636:amyloid beta-protein (25-35); C000606306:PIK3R2 protein, rat; D058543:Class Ia Phosphatidylinositol 3-Kinase; D002118:Calcium
keywords: CCK-8; Calcium detection; Cell viability; PI3K-p85 protein; Soluble beta-amyloid 25–35