Sulbactam protects neurons against double neurotoxicity of amyloid beta and glutamate load by upregulating glial glutamate transporter 1.

ABSTRACT: Amyloid beta (Abeta) synergistically enhances excitotoxicity of glutamate load by impairing glutamate transporter 1 (GLT1) expression and function, which exacerbates the development of Alzheimer's disease (AD). Our previous studies suggested that sulbactam can upregulate the expression levels and capacity of GLT1. Therefore, this study aims to investigate whether sulbactam improves neuronal tolerance against neurotoxicity of Abeta and glutamate load by up-regulating GLT1 in primary neuron-astrocyte co-cultures. Early postnatal P0-P1 Wistar rat pups' cortices were collected for primary neuron-astrocyte cultures. Hoechst-propidium iodide (HO-PI) stain and lactate dehydrogenase (LDH) assays were used to analyze neuronal death. Cell counting kit 8 (CCK8) was applied to determine cell viability

SUBMITTER: Li L 

PROVIDER: S-EPMC10847450 | biostudies-literature | 2024 Feb

REPOSITORIES: biostudies-literature