Metabolic Brain Disease, Journal Year: 2024, Volume and Issue: 40(1)
Published: Nov. 18, 2024
Language: Английский
Metabolic Brain Disease, Journal Year: 2024, Volume and Issue: 40(1)
Published: Nov. 18, 2024
Language: Английский
Journal of Advanced Research, Journal Year: 2024, Volume and Issue: 66, P. 251 - 265
Published: Jan. 7, 2024
The incessant communication that takes place between microglia and neurons is essential the development, maintenance, pathogenesis of central nervous system (CNS). As mobile phagocytic cells, serve a critical role in surveilling scavenging neuronal milieu to uphold homeostasis.
Language: Английский
Citations
15Life Sciences, Journal Year: 2025, Volume and Issue: 363, P. 123392 - 123392
Published: Jan. 11, 2025
Language: Английский
Citations
1Free Radical Biology and Medicine, Journal Year: 2025, Volume and Issue: unknown
Published: April 1, 2025
Language: Английский
Citations
0Probiotics and Antimicrobial Proteins, Journal Year: 2025, Volume and Issue: unknown
Published: April 26, 2025
Spinal cord injury (SCI) disrupts gut flora and exacerbates neuroinflammation. Evidence supports the important role of intestinal microbiota in SCI. This study evaluated neuroprotective effect Limosilactobacillus reuteri (L. reuteri) DSM 17938 on SCI its potential anti-inflammatory mechanism. The was disorganised following SCI, with a significant decrease abundance probiotic bacteria such as L. reuteri. DSM17938 treatment improved spinal pathology enhanced locomotor functional recovery SCI-model rats. Moreover, it modulated tryptophan metabolism by promoting indole-3-carboxaldehyde production. In addition, inhibits polarization M1 microglia reduces production IL-6, IL-1 β, TNF-α to alleviate It also activates aryl hydrocarbon receptor (AhR) signalling via upregulating AhR CYP1A1 expression, tight junction protein synthesis. summary, promotes modulating activate barrier repair attenuate microglial activation neuroinflammation, suggesting strategy for clinical adjuvant treatment.
Language: Английский
Citations
0CNS Neuroscience & Therapeutics, Journal Year: 2024, Volume and Issue: 30(7)
Published: July 1, 2024
We aimed to confirm the inhibitory effect of nicotinamide on fibrotic scar formation following spinal cord injury in mice using functional metabolomics.
Language: Английский
Citations
2Biomolecules, Journal Year: 2024, Volume and Issue: 14(10), P. 1254 - 1254
Published: Oct. 4, 2024
There is significant communication and interdependence among the gut, microbiome, brain during development. Diseases, such as necrotizing enterocolitis (NEC), highlight how injury to immature gastrointestinal tract leads long-term neurological consequences, due vulnerabilities of in early stages life. A better understanding developing gut–microbiota–brain axis needed both prevent treat devastating consequences these disease processes. The a bidirectional pathway that includes metabolic, nervous, endocrine, immune components. In this review, we discuss gut development, microbiome colonization maturation, interactions influence neurodevelopment context NEC. We describe components gut–brain an integral member relationship. Finally, explore derangements within affect normal development function other systems neurodevelopmental for patients.
Language: Английский
Citations
2Neurobiology of Disease, Journal Year: 2024, Volume and Issue: unknown, P. 106742 - 106742
Published: Nov. 1, 2024
Language: Английский
Citations
2Critical Reviews in Food Science and Nutrition, Journal Year: 2024, Volume and Issue: unknown, P. 1 - 13
Published: Dec. 13, 2024
Acrylamide (AA), a compound formed during the thermal processing of high-carbohydrate foods, has been implicated in onset and progression neurodegenerative diseases. An increasing number reports support that gut microbiota plays significant role brain function diseases, suggesting it may act as mediator between AA exposure development Available studies have shown intake affects composition integrity intestinal barrier, both which are often thought to be associated with pathogenesis given numerous evidences linking brain. Based on current understanding, this paper discusses induces diseases by disrupting structure barrier. Furthermore, explores interaction probiotics exposure, well potential for polysaccharides polyphenols improve microenvironment, provides novel perspectives modulating caused through diet.
Language: Английский
Citations
2International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(23), P. 12637 - 12637
Published: Nov. 25, 2024
Neurodegeneration is preeminent in many neurological diseases, and still a major burden we fail to manage patient's care. Its pathogenesis complicated, intricate, far from being completely understood. Taking multiple sclerosis as an example, propose that neurodegeneration neither cause nor consequence by itself. Mitochondrial dysfunction, leading energy deficiency ion imbalance, plays key role neurodegeneration, partly caused the oxidative stress generated microglia astrocytes. Nodal paranodal disruption, with or without myelin alteration, further involved. Myelin loss exposes axons directly inflammatory environment. Moreover, oligodendrocytes provide singular metabolic trophic support axons, but do not emerge unscathed pathological events, primary defects cell apoptosis secondary neuroinflammation axonal damage. Hereby, failure might be overlooked contributor neurodegeneration. Thus, complex interplay between neuroinflammation, demyelination, wherein each primarily secondarily involved, offer more comprehensive understanding of help establishing novel therapeutic strategies for diseases beyond.
Language: Английский
Citations
1Journal of Cellular and Molecular Medicine, Journal Year: 2024, Volume and Issue: 28(24)
Published: Dec. 1, 2024
ABSTRACT Indole‐3‐carboxaldehyde (ICA), a microbiota‐derived tryptophan metabolite, has been reported to protect against atherosclerosis. However, the molecular mechanisms for its atheroprotective effect remain largely unknown. This study aimed explore influence of ICA on lipid accumulation and inflammatory response in THP‐1 macrophage‐derived foam cells. Our results showed that administration upregulated expression miR‐1271‐5p, ATP binding cassette transporter A1 (ABCA1) ABCG1, downregulated histone deacetylase 9 (HDAC9) inhibited macrophage accumulation. treatment also facilitated polarisation M2 phenotype alleviated response, as evidenced by decreased IL‐6 levels increased IL‐10 levels. HDAC9 was identified direct target miR‐1271‐5p. overexpression or miR‐1271‐5p knockdown ABCA1 ABCG1 well response. Taken together, these suggest can suppress mitigate macrophages activating miR‐1271‐5p/HDAC9 signalling cascade, thereby providing new explanations how reduces
Language: Английский
Citations
1