Inhibiting ceramide synthase 5 expression in microglia decreases neuroinflammation after spinal cord injury DOI Creative Commons
Wei Zhang, Yubao Lu, Ruoqi Shen

и другие.

Neural Regeneration Research, Год журнала: 2024, Номер 20(10), С. 2955 - 2968

Опубликована: Июнь 3, 2024

JOURNAL/nrgr/04.03/01300535-202510000-00026/figure1/v/2024-11-26T163120Z/r/image-tiff Microglia, the resident monocyte of central nervous system, play a crucial role in response to spinal cord injury. However, precise mechanism remains unclear. To investigate molecular mechanisms by which microglia regulate neuroinflammatory injury, we performed single-cell RNA sequencing dataset analysis, focusing on changes microglial subpopulations. We found that MG1 subpopulation emerged acute/subacute phase injury and expressed genes related cell pyroptosis, sphingomyelin metabolism, neuroinflammation at high levels. Subsequently, established mouse model contusive intrathecal injection siRNA inhibitors validate ceramide synthase 5 responses pyroptosis after Finally, PC12-BV2 co-culture system pyroptosis-associated proteins were highly induce apoptosis neuron cells. Inhibiting expression effectively reduced pyroptosis. Furthermore, 5-induced was dependent activation NLRP3 signaling pathway. vivo neuronal promoted recovery neurological function. Pla2g7 formed “bridge” between sphingolipid metabolism 5-mediated death inhibiting Collectively, these findings suggest suppressed mediated NLRP3, thereby exerting neuroprotective effects.

Язык: Английский

Neuronal regulated cell death in aging-related neurodegenerative diseases: key pathways and therapeutic potentials DOI Creative Commons
Run Song, Shiyi Yin, Jiannan Wu

и другие.

Neural Regeneration Research, Год журнала: 2024, Номер 20(8), С. 2245 - 2263

Опубликована: Июль 29, 2024

Regulated cell death (such as apoptosis, necroptosis, pyroptosis, autophagy, cuproptosis, ferroptosis, disulfidptosis) involves complex signaling pathways and molecular effectors, has been proven to be an important regulatory mechanism for regulating neuronal aging death. However, excessive activation of regulated may lead the progression aging-related diseases. This review summarizes recent advances in understanding seven forms age-related Notably, newly identified ferroptosis cuproptosis have implicated risk cognitive impairment neurodegenerative These exacerbate disease by promoting inflammation, oxidative stress, pathological protein aggregation. The also provides overview key crosstalk mechanisms among these forms, with a focus on disulfidptosis. For instance, FDX1 directly induces copper ion valency dihydrolipoamide S-acetyltransferase aggregation, while mediates glutathione peroxidase 4 degradation, enhancing sensitivity. Additionally, inhibiting Xc- transport system prevent can increase disulfide formation shift NADP + /NADPH ratio, transitioning insights help uncover potential connections novel differentiate them from traditional mechanisms. In conclusion, identifying targets their points various aid developing specific biomarkers reverse clock treat conditions.

Язык: Английский

Процитировано

4
Advancements in the preparation technology of small molecule artificial antigens and their specific antibodies: a comprehensive review DOI
Yaya Chen, Shuo Ma, Meiling Zhou

и другие.

The Analyst, Год журнала: 2024, Номер 149(18), С. 4583 - 4599

Опубликована: Янв. 1, 2024

Small molecules find extensive application in medicine, food safety, and environmental studies, particularly biomedicine. Immunoassay technology, leveraging the specific recognition between antigens antibodies, offers a superior alternative to traditional physical chemical analysis methods. This approach allows for rapid accurate detection of small molecular compounds, owing its high sensitivity, specificity, swift analytical capabilities. However, compounds often struggle effectively stimulate an immune response due their low weight, weak antigenicity, limited antigenic epitopes. To overcome this, coupling molecule with macromolecular carriers form complete is typically required induce antibodies animals. Consequently, preparation small-molecule artificial production efficient are crucial achieving precise immunoassays. paper reviews recent advancements antibody emphasizing design synthesis haptens, haptens carriers, purification identification antigens, antibodies. Additionally, it evaluates current technological shortcomings limitations while projecting future trends antigen technology.

Язык: Английский

Процитировано

4
Potential therapeutic targets for Alzheimer’s disease: Fibroblast growth factors and their regulation of ferroptosis, pyroptosis and autophagy DOI
Yiwei Li,

Chenbo Yang,

Xiaonan Liu

и другие.

Neuroscience, Год журнала: 2025, Номер unknown

Опубликована: Март 1, 2025

Язык: Английский

Процитировано

0
Neuroinflammation—A Crucial Factor in the Pathophysiology of Depression—A Comprehensive Review DOI Creative Commons

Andreea Sălcudean,

Cristina-Raluca Bodo,

Ramona Amina Popovici

и другие.

Biomolecules, Год журнала: 2025, Номер 15(4), С. 502 - 502

Опубликована: Март 30, 2025

Depression is a multifactorial psychiatric condition with complex pathophysiology, increasingly linked to neuroinflammatory processes. The present review explores the role of neuroinflammation in depression, focusing on glial cell activation, cytokine signaling, blood–brain barrier dysfunction, and disruptions neurotransmitter systems. article highlights how inflammatory mediators influence brain regions implicated mood regulation, such as hippocampus, amygdala, prefrontal cortex. further discusses involvement hypothalamic–pituitary–adrenal (HPA) axis, oxidative stress, kynurenine pathway, providing mechanistic insights into chronic inflammation may underlie emotional cognitive symptoms depression. bidirectional relationship between depressive emphasized, along peripheral immune responses systemic stress. By integrating molecular, cellular, neuroendocrine perspectives, this supports growing field immunopsychiatry lays foundation for novel diagnostic biomarkers anti-inflammatory treatment approaches Further research holds promise developing more effective personalized interventions individuals suffering from

Язык: Английский

Процитировано

0
Targeting UAF1 Alleviate Neurotoxicity by Inhibiting APP/NLRP3 Axis-Mediated Pyroptosis and Apoptosis DOI Creative Commons

Ling Cheng,

Xianguang Meng,

Dandan Tian

и другие.

Neurochemical Research, Год журнала: 2025, Номер 50(2)

Опубликована: Апрель 1, 2025

Язык: Английский

Процитировано

0
Noise exposure-induced the cerebral alterations: From emerging evidence to antioxidant-mediated prevention and treatment DOI Creative Commons
Yuyan Chen, Jie Huang,

Zhiying Zhou

и другие.

Ecotoxicology and Environmental Safety, Год журнала: 2024, Номер 288, С. 117411 - 117411

Опубликована: Ноя. 25, 2024

Язык: Английский

Процитировано

1
FUBP3 mediates the amyloid-β-induced neuronal NLRP3 expression DOI Creative Commons
Jing Yao, Yuan Li,

Xi Liu

и другие.

Neural Regeneration Research, Год журнала: 2024, Номер 20(7), С. 2068 - 2083

Опубликована: Май 10, 2024

JOURNAL/nrgr/04.03/01300535-202507000-00028/figure1/v/2024-09-09T124005Z/r/image-tiff Alzheimer’s disease is characterized by deposition of amyloid-β, which forms extracellular neuritic plaques, and accumulation hyperphosphorylated tau, aggregates to form intraneuronal neurofibrillary tangles, in the brain. The NLRP3 inflammasome may play a role transition from amyloid-β tau phosphorylation aggregation. Because primarily found brain microglia, predominantly located neurons, it has been suggested that expressed microglia indirectly triggers upregulating expression pro-inflammatory cytokines. Here, we neurons also express vitro vivo , neuronal regulates phosphorylation. Using biochemical methods, mapped minimal promoter identified FUBP3 as transcription factor regulating neurons. In primary neuroblastoma cell line Neuro2A, required for endogenous only when present. brains aged wild-type mice mouse model disease, was markedly increased cortical Transcriptome analysis plays neuron-mediated immune responses. We trimmed 5′ end DNA fragments bound, implying functions stress-induced These findings suggest be more directly involved amyloid-β-to–phospho-tau than microglial NLRP3, fundamentally alters regulatory mechanism Given at low levels young strongly upregulated mice, could safe therapeutic target preventing progression.

Язык: Английский

Процитировано

0
EGB761 ameliorates mild cognitive impairment by inhibiting the pyroptosis and apoptosis in both in vivo and in vitro experiments DOI
Xiaolu Zhang,

Yingxin Sun,

Yujia Zheng

и другие.

Archiv der Pharmazie, Год журнала: 2024, Номер unknown

Опубликована: Сен. 17, 2024

Abstract Mild cognitive impairment (MCI) is a neurodegenerative condition that clinically prevalent among the elderly. EGB761 widely recognized for its promising therapeutic properties in both prevention and treatment of disorders. The aim this study was to investigate effects MCI underlying molecular mechanism. Four‐month‐old SAMP8 mice were used as an vivo model, BV2 microglial cells treated with β‐amyloid (Aβ) 1–42 establish vitro model. First, function evaluated by Morris water maze. Then, Aβ levels measured enzyme‐linked immunosorbent assay. Finally, mechanism investigated vitro. It found improved mice. In addition, inhibited NOD‐like receptor protein 3 inflammasome‐mediated pyroptosis‐related mRNAs proteins reduced pyroptosis markers, including gasdermin D fluorescence intensity, propidium iodide‐positive cell count, lactate dehydrogenase content. Furthermore, extrinsic intrinsic apoptosis. Thus, had protective against apoptosis induced Aβ1‐42

Язык: Английский

Процитировано

0
Inhibiting ceramide synthase 5 expression in microglia decreases neuroinflammation after spinal cord injury DOI Creative Commons
Wei Zhang, Yubao Lu, Ruoqi Shen

и другие.

Neural Regeneration Research, Год журнала: 2024, Номер 20(10), С. 2955 - 2968

Опубликована: Июнь 3, 2024

JOURNAL/nrgr/04.03/01300535-202510000-00026/figure1/v/2024-11-26T163120Z/r/image-tiff Microglia, the resident monocyte of central nervous system, play a crucial role in response to spinal cord injury. However, precise mechanism remains unclear. To investigate molecular mechanisms by which microglia regulate neuroinflammatory injury, we performed single-cell RNA sequencing dataset analysis, focusing on changes microglial subpopulations. We found that MG1 subpopulation emerged acute/subacute phase injury and expressed genes related cell pyroptosis, sphingomyelin metabolism, neuroinflammation at high levels. Subsequently, established mouse model contusive intrathecal injection siRNA inhibitors validate ceramide synthase 5 responses pyroptosis after Finally, PC12-BV2 co-culture system pyroptosis-associated proteins were highly induce apoptosis neuron cells. Inhibiting expression effectively reduced pyroptosis. Furthermore, 5-induced was dependent activation NLRP3 signaling pathway. vivo neuronal promoted recovery neurological function. Pla2g7 formed “bridge” between sphingolipid metabolism 5-mediated death inhibiting Collectively, these findings suggest suppressed mediated NLRP3, thereby exerting neuroprotective effects.

Язык: Английский

Процитировано

0