Flavonoid quercetin reduces gliosis after repetitive mild traumatic brain injury in mice

Zabenko, Y.Y.; Pivneva, T. A.

doi:10.15407/fz62.05.050

Cited by 9 publications

(5 citation statements)

References 24 publications

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“…Its reductor effect occurs when it donates a proton and becomes a radical itself, resulting in an unpaired electron delocalized by resonance, making the radical too low in energy to be reactive. It is known that the three structural groups in quercetin have the ability to remain as antioxidants when reacting with free radicals: the B ring o-dihydroxyl groups, the 4-oxo group in conjugation with the 2,3-alkene, and the 3- and 5-hydroxyl groups [ 157 , 158 , 159 , 160 , 161 ].…”

Section: Protective Role Of Antioxidants In Gliosismentioning

confidence: 99%

Trends in Gliosis in Obesity, and the Role of Antioxidants as a Therapeutic Alternative

et al. 2022

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Obesity remains a global health problem. Chronic low-grade inflammation in this pathology has been related to comorbidities such as cognitive alterations that, in the long term, can lead to neurodegenerative diseases. Neuroinflammation or gliosis in patients with obesity and type 2 diabetes mellitus has been related to the effect of adipokines, high lipid levels and glucose, which increase the production of free radicals. Cerebral gliosis can be a risk factor for developing neurodegenerative diseases, and antioxidants could be an alternative for the prevention and treatment of neural comorbidities in obese patients. Aim: Identify the immunological and oxidative stress mechanisms that produce gliosis in patients with obesity and propose antioxidants as an alternative to reducing neuroinflammation. Method: Advanced searches were performed in scientific databases: PubMed, ProQuest, EBSCO, and the Science Citation index for research on the physiopathology of gliosis in obese patients and for the possible role of antioxidants in its management. Conclusion: Patients with obesity can develop neuroinflammation, conditioned by various adipokines, excess lipids and glucose, which results in an increase in free radicals that must be neutralized with antioxidants to reduce gliosis and the risk of long-term neurodegeneration.

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Section: Protective Role Of Antioxidants In Gliosismentioning

confidence: 99%

Trends in Gliosis in Obesity, and the Role of Antioxidants as a Therapeutic Alternative

et al. 2022

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“…The sagittal sections of the brain (50 μm thick) were cut on a vibratome VT1000A (Leica, Wetzlar, Germany). Immunohistochemical staining of astrocytic cells was performed as previously described ( Zabenko and Pivneva, 2016 ). Then hippocampus slices were washed with 0.1 M PB and blocked in 0.1 M PB containing 0.3% Triton X-100 and 0.5% bovine serum albumin.…”

Section: Methodsmentioning

confidence: 99%

Reaction of different cell types of the brain on neurotoxin cuprizone and hormone melatonin treatment in young and aging mice

Labunets

Rodnichenko

Savosko

et al. 2023

Front. Cell. Neurosci.

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IntroductionThe brain myelin and neurons destruction in multiple sclerosis may be associated with the production of neuroinflammatory cells (macrophages, astrocytes, T-lymphocytes) of pro-inflammatory cytokines and free radicals. The age-associated changes of the above cells can influence on the response of nervous system cells to toxic damaging and regulatory factors of humoral/endocrine nature, in particular pineal hormone melatonin. The study aim was (1) to evaluate changes of the brain macrophages, astrocytes, T-cells, neural stem cells, neurons, and central nervous system (CNS) functioning in the neurotoxin cuprizone-treated mice of different age; and (2) to assess in such mice the effects of exogenous melatonin and possible courses of its action.MethodsA toxic demyelination and neurodegeneration model was induced in 129/Sv mice aged 3–5 and 13–15 months by adding cuprizone neurotoxin to their food for 3 weeks. From the 8th day of the cuprizone treatment, melatonin was injected intraperitoneally at 6 p.m. daily, at a dose of 1 mg/kg. The brain GFPA + -cells were evaluated by immunohistochemical method, the proportion of CD11b+, CD3+CD11b+, CD3+, CD3+CD4+, CD3+CD8+, Nestin+-cells was determined via flow cytometry. Macrophage activity was evaluated by their ability to phagocytose latex beads Morphometric analysis of the brain neurons and the behavioral reactions (“open field” and rotarod tests) were performed. To assess the involvement of the bone marrow and thymus in the action of melatonin, the amount of granulocyte/macrophage colony-forming cells (GM-CFC), and blood monocytes and thymic hormone thymulin were evaluated.Results and discussionThe numbers of the GFAP+-, CD3+-, CD3+CD4+, CD3+CD8+, CD11b+, CD3+CD11b+, Nestin+-cells and macrophages phagocytic latex beads and malondialdehyde (MDA) content were increased in the brain of young and aging mice under cuprizone influence. The proportion of undamaged neurons within the brain, motor, affective, and exploratory activities, and muscle tone decreased in mice of both ages. Introducing melatonin to mice of any age reduced the number of GFAP+-, CD3+- cells and their subpopulations, macrophage activation, and MDA content. At the same time, the percentage of brain neurons that were unchanged increased as the number of Nestin+ cells decreased. The behavioral responses were also improved. Besides, the number of bone marrow GM-CFC and the blood level of monocytes and thymulin increased. The effects of both neurotoxin and melatonin on the brain astrocytes, macrophages T-cells, and immune system organs as well as the structure and functioning of neurons were more pronounced in the young mice.ConclusionWe have observed the involvement of the astrocytes, macrophages, T-cells, neural stem cells, and neurons in the brain reaction of mice different age after administration of neurotoxin cuprizone and melatonin. The brain cell composition reaction has the age features. The neuroprotective effects of melatonin in cuprizone-treated mice have been realized through an improvement of the brain cell composition and oxidative stress factors and functioning of bone marrow and thymus.

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“…While the functional significance of this association remains unclear, intraperitoneal administration of dasatinib decreased inflammation, reduced neurodegeneration, and improved neurological outcomes, as compared to placebo control ( Yu et al, 2016 ). Quercetin also provided beneficial effects in rodent models of TBI, reducing oxidative stress after moderate fluid percussion injury ( Schultke et al, 2005 ), improving mitochondrial function and cognitive function after weight drop injury ( Yang et al, 2014 ; Li et al, 2016a ; Li et al, 2016b ), and reducing gliosis and anxious behavior after repetitive mild TBI in mice and rats ( Zabenko and Pivneva, 1994 ; Kosari-Nasab et al, 2019 ; Du et al, 2016 ; Du et al, 2018 ; Song et al, 2021 ); however, it remains undetermined whether these beneficial effects are due to the direct free radical scavenging properties of quercetin or whether these changes are due to downstream senolytic activity. The clinical utility of dasatinib and quercetin remains unexplored in TBI patients; however, Enzogenol, a quercetin containing extract derived from Pinus radiata bark, was safe, well tolerated, and appeared to improve cognitive function, enhance sleep quality, and reduce mental fatigue for up to one year after mild TBI ( Theadom et al, 2013 ; Walter et al, 2017 ).…”

Section: Senotherapeutics – the Future Of Chronic Tbi Managementmentioning

confidence: 99%

Inflammaging, cellular senescence, and cognitive aging after traumatic brain injury

Jarrahi

Moore

et al. 2023

Neurobiology of Disease

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Flavonoid quercetin reduces gliosis after repetitive mild traumatic brain injury in mice

Cited by 9 publications

References 24 publications

Trends in Gliosis in Obesity, and the Role of Antioxidants as a Therapeutic Alternative

Trends in Gliosis in Obesity, and the Role of Antioxidants as a Therapeutic Alternative

Reaction of different cell types of the brain on neurotoxin cuprizone and hormone melatonin treatment in young and aging mice

Inflammaging, cellular senescence, and cognitive aging after traumatic brain injury

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