Neuroscience, Год журнала: 2023, Номер 537, С. 93 - 104
Опубликована: Дек. 5, 2023
Язык: Английский
Ageing Research Reviews, Год журнала: 2023, Номер 93, С. 102160 - 102160
Опубликована: Дек. 7, 2023
Язык: Английский
Процитировано
45
Biomedicines, Год журнала: 2024, Номер 12(3), С. 501 - 501
Опубликована: Фев. 23, 2024
Stroke is a major contributor to global mortality and disability. While reperfusion essential for preventing neuronal death in the penumbra, it also triggers cerebral ischemia-reperfusion injury, paradoxical injury primarily caused by oxidative stress, inflammation, blood–brain barrier disruption. An burst inflicts marked cellular damage, ranging from alterations mitochondrial function lipid peroxidation activation of intricate signalling pathways that can even lead cell death. Thus, given pivotal role stress mechanisms reinforcement antioxidant defence system has been proposed as protective approach. Although this strategy proven be successful experimental models, its translation into clinical practice yielded inconsistent results. However, should considered availability numerous molecules with wide range chemical properties affect extent injury; several groups molecules, including polyphenols, carotenoids, vitamins, among other compounds, mitigate damage intervening multiple at various stages. Multiple trials have previously conducted evaluate these using melatonin, acetyl-L-carnitine, chrysanthemum extract, edaravone dexborneol, saffron, coenzyme Q10, oleoylethanolamide, treatments. Therefore, multi-antioxidant therapy emerges promising novel therapeutic option due potential synergistic effect provided simultaneous roles individual compounds.
Язык: Английский
Процитировано
15
Journal of Inflammation Research, Год журнала: 2024, Номер Volume 17, С. 3335 - 3352
Опубликована: Май 1, 2024
Abstract: Ischemic stroke is the most common type of stroke, which main cause death and disability on a global scale. As primary immune cells in brain that are crucial for preserving homeostasis central nervous system microenvironment, microglia have been found to exhibit dual or even multiple effects at different stages ischemic stroke. The anti-inflammatory polarization release neurotrophic factors may provide benefits by promoting neurological recovery lesion early phase after However, pro-inflammatory secretion inflammatory later injury exacerbate lesion, suggesting therapeutic potential modulating balance microglial predispose them transformation Microglia-mediated signaling crosstalk with other also be key improving functional outcomes following Thus, this review provides an overview functions responses under physiological conditions, including activation, polarization, interactions cells. We focus approaches promote microglia, inhibit enhance beneficial cell-to-cell interactions. These targets hold promise creation innovative strategies. Keywords: phagocytosis, crosstalk, anti-inflammatory,
Язык: Английский
Процитировано
15
Journal of Translational Medicine, Год журнала: 2024, Номер 22(1)
Опубликована: Янв. 2, 2024
NAD(P)H Quinone Dehydrogenase 1 (NQO1) plays a pivotal role in the regulation of neuronal function and synaptic plasticity, cellular adaptation to oxidative stress, neuroinflammatory degenerative processes, tumorigenesis central nervous system (CNS). Impairment NQO1 activity CNS can result abnormal neurotransmitter release clearance, increased aggravated injury/death. Furthermore, it cause disturbances neural circuit neurotransmission. The abnormalities enzyme have been linked pathophysiological mechanisms multiple neurological disorders, including Parkinson's disease, Alzheimer's epilepsy, sclerosis, cerebrovascular traumatic brain injury, malignancy. contributes various dimensions treatment response tumors. precise through which contribute these disorders continue be subject ongoing research. Building upon existing knowledge, present study reviews current investigations describing dysregulations disorders. This emphasizes potential as biomarker diagnostic prognostic approaches, well its suitability target for drug development strategies
Язык: Английский
Процитировано
14
Molecular Neurobiology, Год журнала: 2024, Номер 61(9), С. 6161 - 6174
Опубликована: Янв. 27, 2024
Язык: Английский
Процитировано
13
Frontiers in Molecular Neuroscience, Год журнала: 2024, Номер 17
Опубликована: Июнь 12, 2024
Stroke is a devastating disease with high morbidity, disability, and mortality, among which ischemic stroke more common. However, there still lack of effective methods to improve the prognosis reduce incidence its complications. At present, evidence that peripheral organs are involved in inflammatory response after stroke. Moreover, interaction between central inflammation includes activation resident immune cells, as well inflammation-related signaling pathways, all play an important role pathophysiology In this review, we discuss mechanisms stroke, interactions through circulatory pathways (such gut, heart, lung spleen) brain mediate regulate We also propose potential meningeal lymphatic vessels (MLVs)-cervical lymph nodes (CLNs) brain-peripheral crosstalk pathway addition, summarize anti-inflammatory drugs treatment
Язык: Английский
Процитировано
11
Frontiers in Cellular Neuroscience, Год журнала: 2023, Номер 17
Опубликована: Июнь 8, 2023
Stroke ranks second as a leading cause of death and permanent disability globally. Microglia, innate immune cells in the brain, respond rapidly to ischemic injury, triggering robust persistent neuroinflammatory reaction throughout disease’s progression. Neuroinflammation plays critical role mechanism secondary injury stroke is significant controllable factor. Microglia activation takes on two general phenotypes: pro-inflammatory M1 type anti-inflammatory M2 type, although reality more complex. The regulation microglia phenotype crucial controlling response. This review summarized key molecules mechanisms polarization, function, phenotypic transformation following cerebral ischemia, with focus influence autophagy polarization. goal provide reference for development new targets treatment based
Язык: Английский
Процитировано
23
Aging and Disease, Год журнала: 2023, Номер unknown, С. 0 - 0
Опубликована: Янв. 1, 2023
Blood-brain barrier (BBB) damage is the main pathological basis for acute ischemic stroke (AIS)-induced cerebral vasogenic edema and hemorrhagic transformation (HT). Glial cells, including microglia, astrocytes, oligodendrocyte precursor cells (OPCs)/oligodendrocytes (OLs) play critical roles in BBB protection. Recent evidence indicates that immune also have an important role damage, HT. Therefore, regulating crosstalk between glial would hold promise to alleviate AIS-induced damage. In this review, we first introduce of glia pericytes, protection after AIS, emphasizing polarization, inflammatory response other cells. We then describe cell-derived exosomes AIS. Next, specifically discuss Finally, propose could be a potential target alleviating AIS some molecular targets strategies by
Язык: Английский
Процитировано
23
Frontiers in Cellular Neuroscience, Год журнала: 2023, Номер 17
Опубликована: Июнь 2, 2023
Ceramide, a bioactive sphingolipid, serves as an important second messenger in cell signal transduction. Under stressful conditions, it can be generated from de novo synthesis, sphingomyelin hydrolysis, and/or the salvage pathway. The brain is rich lipids, and abnormal lipid levels are associated with variety of disorders. Cerebrovascular diseases, which mainly caused by cerebral blood flow secondary neurological injury, leading causes death disability worldwide. There growing body evidence for close connection between elevated ceramide cerebrovascular especially stroke small vessel disease (CSVD). increased has broad effects on different types cells, including endothelial microglia, neurons. Therefore, strategies that reduce such modifying sphingomyelinase activity or rate-limiting enzyme synthesis pathway, serine palmitoyltransferase, may represent novel promising therapeutic approaches to prevent treat injury-related diseases.
Язык: Английский
Процитировано
21
Journal of Cellular and Molecular Medicine, Год журнала: 2023, Номер 27(12), С. 1653 - 1663
Опубликована: Май 2, 2023
Abstract High‐mobility group box1 (HMGB1) induces inflammatory injury, and emerging reports suggest that it is critical for brain ischemia reperfusion. Engeletin, a natural Smilax glabra rhizomilax derivative, reported to possess anti‐inflammatory activity. Herein, we examined the mechanism of engeletin‐mediated neuroprotection in rats having transient middle cerebral artery occlusion (tMCAO) against reperfusion injury. Male SD were induced using 1.5 h tMCAO, following by 22.5 h. Engeletin (15, 30 or 60 mg/kg) was intravenously administered immediately 0.5 ischemia. Based on our results, engeletin, dose‐dependent fashion, reduced neurological deficits, infarct size, histopathological alterations, edema factors, namely, circulating IL‐1β, TNF‐α, IL‐6 IFN‐γ. Furthermore, engeletin treatment markedly neuronal apoptosis, which, turn, elevated Bcl‐2 protein levels, while suppressing Bax Cleaved Caspase‐3 levels. Meanwhile, significantly reduces overall expressions HMGB1, TLR4, NF‐κB attenuated nuclear transfer factor kappa B (NF‐κB) p65 ischemic cortical tissue. In conclusion, strongly prevents focal via suppression HMGB1/TLR4/NF‐κB network.
Язык: Английский
Процитировано
20