CuO-NPs Induce Apoptosis and Functional Impairment in BV2 Cells Through the CSF-1R/PLCγ2/ERK/Nrf2 Pathway

Toxics, Journal Year: 2025, Volume and Issue: 13(4), P. 231 - 231

Published: March 21, 2025

Copper oxide nanoparticles (CuO-NPs) induce neurological diseases, including neurobehavioral defects and neurodegenerative diseases. Direct evidence indicates that CuO-NPs inflammation in the central nervous system cause severe neurotoxicity. However, mechanism of CuO-NP-induced damage to has rarely been studied, toxicity different CuO-NP particle sizes their copper ion (Cu2+) precipitation microglia (BV2 cells) is worth exploring. Therefore, this study investigated with (small size: S-CuO-NPs; large L-CuO-NPs), Cu2+ equal molar mass (replaced by CuCl2 [Equ group]), precipitated a cell culture solution [Pre examined action each on BV2 after co-culture for 12 h 24 h. The activity cells decreased, morphology was damaged, apoptosis rate increased all exposed groups. Toxicity time- dose-dependently, highest Equ group, followed S-CuO-NPs, L-CuO-NPs, Pre groups, respectively. Subsequently, we S-CuO-NP-induced injury, revealed S-CuO-NPs induced oxidative stress inflammatory response membrane permeability cells. Moreover, reduced ratio p-CSF-1R/CSF-1R, p-PLCγ2/PLCγ2, p-extracellular signal-regulated kinase (ERK)/ERK, p-Nrf2/Nrf2, Bcl-2/Bax protein expression microglia, elevated cleaved caspase-3 expression. CSF-1R/PLCγ2/ERK/Nrf2 apoptotic pathway activated. downregulation CX3CR1, CSF-1R, brain-derived neurotrophic factor (BDNF), IGF-1 impairment repair protection functions system. In summary, our results reveal promote an increase molecules through stress, activate pathway, apoptosis, ultimately result neurofunctional microglia.

Language: Английский

Ageing-related changes in the regulation of microglia and their interaction with neurons

Neuropharmacology, Journal Year: 2024, Volume and Issue: unknown, P. 110241 - 110241

Published: Nov. 1, 2024

Language: Английский