Sevoflurane aggravates cognitive impairment in OSAS mice through tau phosphorylation and mitochondrial dysfunction DOI Creative Commons
Feixiang Li,

Dujuan Li,

Bo Gong

et al.

Experimental Neurology, Journal Year: 2024, Volume and Issue: 384, P. 115056 - 115056

Published: Nov. 12, 2024

With an aging population, the incidence of obstructive sleep apnea syndrome (OSAS) is rising, resulting in a growing number patients undergoing surgery who are also affected by OSAS. The combined impact anesthetic drugs and OSAS-related neurological damage has drawn significant attention. Here, wild-type (WT) Tau-knockout (Tau-KO) mice were subjected to intermittent hypoxia sevoflurane exposure induce OSAS sevoflurane-induced neurotoxicity. Protein expression tau phosphorylation (Tau-Ser202/Thr205 Tau-Ser422) was measured Western blotting. Immunofluorescence used visualize (Tau-Ser202/Thr205) hippocampal CA1 region. Mitochondrial function evaluated measuring reactive oxygen species (ROS), mitochondrial membrane potential (MMP), ATP levels. Cognitive functions assessed using Morris water maze Y-maze tests. We found that compared WT group, significantly increased dysfunction mice, leading cognitive impairment. Interestingly, idebenone treatment mitigated impairment but it did not affect phosphorylation. Compared Tau-KO control exhibited impairment, exacerbate or these mice. These findings suggest exacerbates impairments through phosphorylation-induced dysfunction, uncovered differing mechanisms between induced those exacerbated sevoflurane.

Language: Английский

Idebenone improves mitochondrial respiratory activity and attenuates oxidative damage via the SIRT3-SOD2 pathway in a prion disease cell model DOI

Zhixin Sun,

Pei Wen,

Dongming Yang

et al.

Life Sciences, Journal Year: 2025, Volume and Issue: 366-367, P. 123481 - 123481

Published: Feb. 19, 2025

Language: Английский

Citations

0
Novel idebenone derivatives attenuated oxidative stress injury and myocardial damage DOI Creative Commons
Yuwei Peng,

Yishan Guo,

Xinyi Yang

et al.

Frontiers in Chemistry, Journal Year: 2025, Volume and Issue: 13

Published: Feb. 24, 2025

Oxidative stress-induced cardiomyocyte apoptosis was the primary causative factor of cardiovascular disease (CVD). However, existing therapy drugs for oxidative stress were much less investigated, which underlined necessity new drug discovery and development. Herein, we aimed to synthesize several novel idebenone (IDE) derivatives investigate protective effect mechanism these against H2O2-induced injury in H9C2 cells by determining cell proliferation rate, detecting reactive oxygen species (ROS) level, expression related proteins. Additionally, study also investigated IDE-1 pretreatment on Balb/c mice after hypoxia-reoxygenation. In vivo experiments, damage cardiomyocytes assessed using hematoxylin-eosin (HE) staining terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining. The results showed that possessed highest antioxidant activity among all IDE derivatives, could notably decrease levels intracellular ROS. Furthermore, confirmed be potentially linked oxidation-related pathway heme oxygenase-1 (HO-1) apoptosis-related Bcl-2/Bax caspase-3. Our demonstrated a research direction treatment diseases associated with stress.

Language: Английский

Citations

0
Q-Der: a next-generation CoQ10 analogue supercharging neuroprotection by combating oxidative stress and enhancing mitochondrial function DOI Creative Commons
Matteo Micucci,

Federico Gianfanti,

Sabrina Donati Zeppa

et al.

Frontiers in Molecular Biosciences, Journal Year: 2025, Volume and Issue: 12

Published: Feb. 25, 2025

Mitochondrial dysfunction and oxidative stress are central mechanisms in the progression of neurodegenerative diseases. This study first evaluated toxicity Q-Der (Q10-diacetate), a derivative Coenzyme Q10, HT22 hippocampal neurons under normal conditions. cells were treated with at 2.5, 5 10 µM without rotenone. superoxide production (Mitosox), gene expression (via qRT-PCR), protein levels Western blot) measured. Morphological analyses performed using transmission (TEM) scanning (SEM) electron microscopes. significantly reduced mitochondrial levels, particularly μM, upregulated key biogenesis genes, including PGC-1α TFAM. Additionally, it restored MT-ND1 MT-COI, which downregulated by blot results showed significant recovery CV-ATP5A (complex V) (p < 0.05), preserving ATP production. further confirmed Q-Der's ability to maintain cellular structure These findings suggest that is non-toxic conditions protects against stress, supporting its potential as therapeutic agent for

Language: Английский

Citations

0
Cognitive impairment in depression and cerebrovascular disease DOI Creative Commons
Igor V. Reverchuk

Neurology neuropsychiatry Psychosomatics, Journal Year: 2025, Volume and Issue: 17(2), P. 107 - 115

Published: April 21, 2025

The treatment of patients with cognitive impairment (CI) remains an urgent problem modern neurology and psychiatrydue to the widespread prevalence CI predicted increase in number future. Among most common reasons for development deficits young are depressive disorders, elderly – vascular disease brain, Alzheimer's their combination. We discuss pathophysiological features depression, possible therapeutic options that allow choose personalized therapy improve quality life patients.

Language: Английский

Citations

0
Sevoflurane aggravates cognitive impairment in OSAS mice through tau phosphorylation and mitochondrial dysfunction DOI Creative Commons
Feixiang Li,

Dujuan Li,

Bo Gong

et al.

Experimental Neurology, Journal Year: 2024, Volume and Issue: 384, P. 115056 - 115056

Published: Nov. 12, 2024

With an aging population, the incidence of obstructive sleep apnea syndrome (OSAS) is rising, resulting in a growing number patients undergoing surgery who are also affected by OSAS. The combined impact anesthetic drugs and OSAS-related neurological damage has drawn significant attention. Here, wild-type (WT) Tau-knockout (Tau-KO) mice were subjected to intermittent hypoxia sevoflurane exposure induce OSAS sevoflurane-induced neurotoxicity. Protein expression tau phosphorylation (Tau-Ser202/Thr205 Tau-Ser422) was measured Western blotting. Immunofluorescence used visualize (Tau-Ser202/Thr205) hippocampal CA1 region. Mitochondrial function evaluated measuring reactive oxygen species (ROS), mitochondrial membrane potential (MMP), ATP levels. Cognitive functions assessed using Morris water maze Y-maze tests. We found that compared WT group, significantly increased dysfunction mice, leading cognitive impairment. Interestingly, idebenone treatment mitigated impairment but it did not affect phosphorylation. Compared Tau-KO control exhibited impairment, exacerbate or these mice. These findings suggest exacerbates impairments through phosphorylation-induced dysfunction, uncovered differing mechanisms between induced those exacerbated sevoflurane.

Language: Английский

Citations

0