Protective effects of melatonin on stroke in diabetic mice: central and peripheral inflammation modulation DOI Creative Commons
Cuiying Liu, Jiayi Guo, Longfei Guan

и другие.

Stroke and Vascular Neurology, Год журнала: 2025, Номер unknown, С. svn - 003442

Опубликована: Фев. 24, 2025

Background Melatonin protects against ischaemic stroke in diabetic animal models, though the mechanisms involving brain and peripheral immune responses remain underexplored. We aimed to clarify how melatonin interacts with these protect mice. Methods Type 1 diabetes mellitus (T1DM) was induced mice using streptozotocin. RNA sequencing of tissue blood mononuclear cells (PBMCs) performed 24 hours poststroke. Inflammatory were evaluated 72 after ischaemia/reperfusion. Results reduced infarction improved neurological function T1DM In brain, downregulated inflammatory factor expression, bioinformatics identifying 62 differentially expressed genes (DEGs) related inflammation 11 associated inflammasomes. Western blotting confirmed reductions NLRP3, HMGB1 Cleaved Caspase-1 expression. Flow cytometry showed infiltration CD8+T neutrophils. decreased IL-6, IL-1β IL-4 levels. PBMCs, revealed 939 DEGs following treatment. Kyoto Encyclopaedia Genes Genomes analysis indicated that involved metabolic pathways, upregulated enriched Jak-STAT signalling pathway. GO cytosol, macromolecule modification. Protein–protein interaction affected 38 inflammation-associated linked key cytokines (Il6, Il1b, Ifng, Il4). increased cells, monocytes neutrophils blood, suggesting a reversal immunosuppression. Multiplex cytokine assays IL-6 IFN-γ Conclusion Poststroke therapy reduces damage by modulating central responses.

Язык: Английский

Stroke in the Time of Circadian Medicine DOI Open Access
Philipp Mergenthaler, Joyce S. Balami, Ain Neuhaus

и другие.

Circulation Research, Год журнала: 2024, Номер 134(6), С. 770 - 790

Опубликована: Март 14, 2024

Time-of-day significantly influences the severity and incidence of stroke. Evidence has emerged not only for circadian governance over stroke risk factors, but also important determinants clinical outcome. In this review, we provide a comprehensive overview interplay between chronobiology cerebrovascular disease. We discuss regulation pathophysiological mechanisms underlying onset or tolerance as well in vascular dementia. This includes cell death mechanisms, metabolism, mitochondrial function, inflammation/immunity. Furthermore, present evidence supporting link disrupted rhythms increased susceptibility to propose that biochemical physiological pathways brain increase damage after sleep attenuate treatment effectiveness during active phase. review underscores importance considering biology understanding pathology choice dementia speculates patient's chronotype may be an factor developing precision following

Язык: Английский

Процитировано

7

Exposure to Environmental Toxins: Potential Implications for Stroke Risk via the Gut– and Lung–Brain Axis DOI Creative Commons

Alexandria Ruggles,

Corinne Benakis

Cells, Год журнала: 2024, Номер 13(10), С. 803 - 803

Опубликована: Май 8, 2024

Recent evidence indicates that exposure to environmental toxins, both short-term and long-term, can increase the risk of developing neurological disorders, including neurodegenerative diseases (i.e., Alzheimer's disease other dementias) acute brain injury stroke). For stroke, latest systematic analysis revealed ambient particulate matter is second most frequent stroke after high blood pressure. However, preclinical clinical investigations on deleterious consequences pollutants are scarce. This review examines recent how absorbed along digestive tract or inhaled through lungs, affect host cellular response. We particularly address toxins immune response microbiome at gut lung barrier sites. Additionally, this highlights findings showing potential contribution an increased stroke. A better understanding biological mechanisms underlying has mitigate disorders.

Язык: Английский

Процитировано

7

Retinoic acid alleviates the reduction of Akt and Bad phosphorylation and regulates Bcl-2 family protein interactions in animal models of ischemic stroke DOI Creative Commons
Ju-Bin Kang, Phil‐Ok Koh

PLoS ONE, Год журнала: 2024, Номер 19(5), С. e0303213 - e0303213

Опубликована: Май 16, 2024

Ischemic stroke causes a lack of oxygen and glucose supply to brain, eventually leads severe neurological disorders. Retinoic acid is major metabolic product vitamin A has various biological effects. The PI3K-Akt signaling pathway an important survival in brain. Phosphorylated Akt regulating apoptosis. We examined whether retinoic neuroprotective effects model by its downstream protein, Bad. Moreover, we investigated the relationship between Bcl-2 family protein interactions. Animals were intraperitoneally administered vehicle or (5 mg/kg) for four days before surgery ischemic was induced middle cerebral artery occlusion (MCAO) surgery. Neurobehavioral tests performed 24 h after MCAO cortical tissues collected. Cresyl violet staining TUNEL histochemistry performed, Western blot immunoprecipitation analysis elucidate expression proteins. reduced deficits histopathological changes, decreased number TUNEL-positive cells, alleviated reduction phospho-PDK1, phospho-Akt, phospho-Bad caused damage. Immunoprecipitation showed that damage interaction 14-3-3, which attenuated acid. Furthermore, mitigated increase Bcl-2/Bad Bcl-xL/Bad binding levels Bcl-2/Bax Bcl-xL/Bax MCAO-induced caspase-3 cleaved expression. demonstrate prevented apoptosis against ischemia through phosphorylation Bad, maintenance 14-3-3 binding, regulation .

Язык: Английский

Процитировано

7

Landscape of stroke comorbidities DOI
Ming Zheng,

Carl J Lavie

Progress in Cardiovascular Diseases, Год журнала: 2024, Номер 86, С. 96 - 99

Опубликована: Сен. 1, 2024

Язык: Английский

Процитировано

7

Protective effects of melatonin on stroke in diabetic mice: central and peripheral inflammation modulation DOI Creative Commons
Cuiying Liu, Jiayi Guo, Longfei Guan

и другие.

Stroke and Vascular Neurology, Год журнала: 2025, Номер unknown, С. svn - 003442

Опубликована: Фев. 24, 2025

Background Melatonin protects against ischaemic stroke in diabetic animal models, though the mechanisms involving brain and peripheral immune responses remain underexplored. We aimed to clarify how melatonin interacts with these protect mice. Methods Type 1 diabetes mellitus (T1DM) was induced mice using streptozotocin. RNA sequencing of tissue blood mononuclear cells (PBMCs) performed 24 hours poststroke. Inflammatory were evaluated 72 after ischaemia/reperfusion. Results reduced infarction improved neurological function T1DM In brain, downregulated inflammatory factor expression, bioinformatics identifying 62 differentially expressed genes (DEGs) related inflammation 11 associated inflammasomes. Western blotting confirmed reductions NLRP3, HMGB1 Cleaved Caspase-1 expression. Flow cytometry showed infiltration CD8+T neutrophils. decreased IL-6, IL-1β IL-4 levels. PBMCs, revealed 939 DEGs following treatment. Kyoto Encyclopaedia Genes Genomes analysis indicated that involved metabolic pathways, upregulated enriched Jak-STAT signalling pathway. GO cytosol, macromolecule modification. Protein–protein interaction affected 38 inflammation-associated linked key cytokines (Il6, Il1b, Ifng, Il4). increased cells, monocytes neutrophils blood, suggesting a reversal immunosuppression. Multiplex cytokine assays IL-6 IFN-γ Conclusion Poststroke therapy reduces damage by modulating central responses.

Язык: Английский

Процитировано

1