The role of oxidative stress in the protective effect of boric acid against glutamate excitotoxicity in C6 glioma cells DOI Open Access
Ayşegül Öztürk, Ahmet Şevki Taşkıran,

Emin Gündoğdu

et al.

Journal of Boron, Journal Year: 2025, Volume and Issue: 10(1), P. 1 - 9

Published: April 1, 2025

This study designed to investigate the biochemical changes in glial cells' oxidant/antioxidant systems response glutamate-induced excitotoxicity of boric acid (BA). The present employed C6 cells. For study, cells were separated into 4 groups as control, glutamate (10mM), glutamate+BA (0,23; 0,46; 0,93; 1,87 and 3,75 μg/mL), BA μg/mL). control group was not treated. treated with 10 mM for 24 hours. administered one hour prior addition incubated viability evaluated using an XTT assay. Commercial kits used analyses. Significance set at less than 0.05. analysis revealed that levels malondialdehyde (MDA), nitric oxide (NO), inducible snythase (iNOS), neuronal synthase (nNOS), total oxidant status (TOS) elevated compared (p

Language: Английский

Vagus nerve stimulation: A targeted approach for reducing tissue-specific ischemic reperfusion injury DOI

Parmeshar Singh,

Manju Chaudhary,

Jacob S Kazmi

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2025, Volume and Issue: 184, P. 117898 - 117898

Published: Feb. 8, 2025

Language: Английский

Citations

0

Puerarin Alleviates Cerebral Ischemia–Reperfusion Injury by Inhibiting Ferroptosis Through SLC7A11/GPX4/ACSL4 Axis and Alleviate Pyroptosis Through Caspase-1/GSDMD Axis DOI
Ying Huang, Jiehong Yang, Ting Lu

et al.

Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown

Published: March 8, 2025

Language: Английский

Citations

0

Activation of the 20S proteasome core particle prevents cell death induced by oxygen- and glucose deprivation in cultured cortical neurons DOI Creative Commons
Ivan L. Salazar,

Michele Curcio,

Miranda Mele

et al.

APOPTOSIS, Journal Year: 2025, Volume and Issue: unknown

Published: March 17, 2025

Abstract Neuronal damage in brain ischemia is characterized by a disassembly of the proteasome and decrease its proteolytic activity. However, to what extent these alterations are coupled neuronal death controversial since inhibitors were shown provide protection different models stroke rodents. This question was addressed present work using cultured rat cerebrocortical neurons subjected transient oxygen- glucose-deprivation (OGD) as model for vitro ischemia. Under latter conditions there time-dependent loss activity, determined cleavage Suc-LLVY-AMC fluorogenic substrate, proteasome, assessed native-polyacrylamide gel electrophoresis followed western blot against Psma2 Rpt6, which components catalytic core regulatory particle, respectively. Immunocytochemistry experiments two proteins also showed differential effects on their dendritic distribution. OGD downregulated protein levels Rpt3 Rpt10, mechanism dependent activity NMDA receptors mediated calpains. Activation an inhibitor USP14, deubiquitinase enzyme, inhibited OGD-induced cell death, decreased calpain analysis spectrin cleavage. Similar results obtained presence oleic amide derivatives (B12 D3) directly activate 20S particle. Together, show that activation prevents cortical ischemia, indicating inhibition mediator

Language: Английский

Citations

0

Mechanisms and strategies for organ recovery DOI
David Andrijević, Ana Spajic, Irbaz Hameed

et al.

Nature Reviews Bioengineering, Journal Year: 2025, Volume and Issue: unknown

Published: March 20, 2025

Language: Английский

Citations

0

The role of oxidative stress in the protective effect of boric acid against glutamate excitotoxicity in C6 glioma cells DOI Open Access
Ayşegül Öztürk, Ahmet Şevki Taşkıran,

Emin Gündoğdu

et al.

Journal of Boron, Journal Year: 2025, Volume and Issue: 10(1), P. 1 - 9

Published: April 1, 2025

This study designed to investigate the biochemical changes in glial cells' oxidant/antioxidant systems response glutamate-induced excitotoxicity of boric acid (BA). The present employed C6 cells. For study, cells were separated into 4 groups as control, glutamate (10mM), glutamate+BA (0,23; 0,46; 0,93; 1,87 and 3,75 μg/mL), BA μg/mL). control group was not treated. treated with 10 mM for 24 hours. administered one hour prior addition incubated viability evaluated using an XTT assay. Commercial kits used analyses. Significance set at less than 0.05. analysis revealed that levels malondialdehyde (MDA), nitric oxide (NO), inducible snythase (iNOS), neuronal synthase (nNOS), total oxidant status (TOS) elevated compared (p

Language: Английский

Citations

0