Neuropharmacology, Journal Year: 2024, Volume and Issue: 259, P. 110118 - 110118
Published: Aug. 15, 2024
Language: Английский
Neuropharmacology, Journal Year: 2024, Volume and Issue: 259, P. 110118 - 110118
Published: Aug. 15, 2024
Language: Английский
International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(10), P. 5085 - 5085
Published: May 7, 2024
The brain is the central organ of adaptation to stress because it perceives and determines threats that induce behavioral, physiological, molecular responses. In humans, chronic manifests as an enduring consistent feeling pressure being overwhelmed for extended duration. This can result in a persistent proinflammatory response peripheral nervous system (CNS), resulting cellular, behavioral effects. Compounding stressors may increase risk chronic-stress-induced inflammation, which yield serious health consequences, including mental disorders. review summarizes current knowledge surrounding neuroinflammatory rodent models stress—a relationship continually defined. Many studies investigating effects on neuroinflammation have identified significant changes inflammatory modulators, nuclear factor-κB (NF-κB) toll-like receptors (TLRs), cytokines, tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, IL-6. suggests these are key factors response, contribute establishment anxiety depression-like symptoms. neurological modulating through gene knockdown (KD) knockout (KO), conventional alternative medicine approaches, discussed.
Language: Английский
Citations
12European Journal of Pharmacology, Journal Year: 2024, Volume and Issue: 978, P. 176763 - 176763
Published: June 20, 2024
Language: Английский
Citations
4Materials Letters, Journal Year: 2025, Volume and Issue: unknown, P. 138189 - 138189
Published: Feb. 1, 2025
Language: Английский
Citations
0Brain Research Bulletin, Journal Year: 2025, Volume and Issue: unknown, P. 111338 - 111338
Published: April 1, 2025
Acute ischemic stroke (AIS) is a focal neurological deficit due to sudden occlusion of cerebral vessels in the brain. AIS-induced neuronal injury and associated excite-toxicity neurodegeneration affect synthesis release different neurotrophic factors such as brain-derived neurotropic factor (BDNF) its precursor proBDNF. Both BDNF proBDNF act on specific receptors with effects. activates tropomyosin receptor kinase B (TrkB) results promoting survival, synaptic plasticity, growth. However, p75 neurotrophin (p75NTR) sortilin which attenuates plasticity promotes apoptosis. Dysregulation central peripheral expression proBDNF/BDNF linked severity clinical outcomes AIS. Therefore, this review aims discuss alterations signaling Findings from present illustrated that proBDNF/p75NTR/sortilin pathway exaggerated whereas; BDNF-TrkB reduced AIS leading activation signaling, inhibition could be promising therapeutic strategy management
Language: Английский
Citations
0Molecular Neurobiology, Journal Year: 2024, Volume and Issue: 62(4), P. 4221 - 4236
Published: Oct. 18, 2024
Depression is recognized globally as one of the most intractable diseases, and its complexity diversity make treatment extremely challenging. Acupuncture has demonstrated beneficial effects in various psychiatric disorders. However, underlying mechanisms acupuncture's antidepressant action, particularly depression, remain elusive. Therefore, this study aimed to investigate acupuncture on chronic unpredictability stress (CUMS)-induced depressive symptoms rats further elucidate molecular mechanisms. All were exposed CUMS two stressors every day for 28 days, except control group. One hour before CUMS, given a with acupuncture, electroacupuncture, sham-acupuncture, or fluoxetine (2.1 mg/kg). Behavioral tests biological detection methods conducted sequence evaluate depression-like phenotype rats. The findings demonstrate that therapy effectively ameliorated behavior induced by Additionally, exerted restorative effect alterations levels malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), brain-derived neurotrophic factor (BDNF), cyclic AMP response element-binding protein (CREB), postsynaptic density95 (PSD95), gamma-aminobutyric acid (GABA), acetylcholine (ACh). our indicate also modulates ERK Caspase-3 apoptotic pathways hippocampus This suggests may play potential preventive role regulating hippocampal neuroinflammatory response, oxidative stress, processes, enhancing synaptic plasticity.
Language: Английский
Citations
2Neuropharmacology, Journal Year: 2024, Volume and Issue: 259, P. 110118 - 110118
Published: Aug. 15, 2024
Language: Английский
Citations
0