Dimethyl phthalate exposure induces cognitive impairment through COX2-mediated microglial activation DOI Creative Commons
Genghuan Wang, Jian Shen,

Yingcong Lin

et al.

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: March 20, 2024

Abstract AIM We investigated the mechanism of action whereby exposure to dimethyl phthalate (DMP), an environmental pollutant, causes cognitive impairment. METHODS Network pharmacology was used analyze targets and regulatory networks associated with DMP-brain injury-cognitive The intake DMP simulated by exposure, Morris water maze adopted examine tissue levels inflammatory cytokines were detected. Brain damage assayed H&E Nissl staining, protein expression identified Western blotting. effects observed after separate application siRNA-COX2 celecoxib-COX2 inhibitors. In in vitro experiment, on microglia activation investigated. RESULTS revealed that PTGS2 (COX2) significantly correlated DMP, which could act through COX2. After mice showed significant brain injury impairment, along upregulation cytokines. inhibit ameliorate impairment mice. results activate cause neuroinflammation. CONCLUSION can induce neuroinflammation COX2-mediated microglia, resulting COX2 is important target for action.

Language: Английский

Echinatin alleviates inflammation and pyroptosis in hypoxic-ischemic brain damage by inhibiting TLR4/ NF-κB pathway DOI

Xiaoyue Tao,

Yingying Hu,

Niping Mao

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 136, P. 112372 - 112372

Published: June 7, 2024

Language: Английский

Citations

8
Astragalin improves cognitive disorder in Alzheimer's disease: Based on network pharmacology and molecular docking simulation DOI Creative Commons
Rui Du, Hongyan Pei, Zhongmei He

et al.

CNS Neuroscience & Therapeutics, Journal Year: 2024, Volume and Issue: 30(8)

Published: Aug. 1, 2024

We investigate the mechanism of action astragalin (AST) in treatment Alzheimer's disease (AD). Network pharmacology was conducted to analyze relationships among AST, AD, and neuroinflammation, The APP/PS1 transgenic mice with AD were used experiments; be specific, influence AST on behavior analyzed by Morris water maze eight-arm radial tests, tissue inflammatory factor levels detected ELISA, pathological changes H&E immunohistochemical staining. Analysis results network suggested that exerted multi-target effect neuroinflammation AD. Through molecular docking dynamics analyses, COX2 might target AST. Moreover, animal experimental demonstrated improved mice, enhanced motor memory abilities, meanwhile, it suppressed expression factors tissues activation microglial cells. this study discovers can suppress cell via improve

Language: Английский

Citations

5
Echinatin inhibits osteoarthritis through the NF-κB signaling pathway DOI Creative Commons

Peng Zhan,

Shiming Huang,

D. Chen

et al.

Naunyn-Schmiedeberg s Archives of Pharmacology, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 2, 2025

Language: Английский

Citations

0
Natural retrochalcones: rare compounds with diverse biological activities DOI Creative Commons
Milan Malaník

Phytochemistry Reviews, Journal Year: 2025, Volume and Issue: unknown

Published: March 11, 2025

Language: Английский

Citations

0
Vortioxetine alleviates motor, cognitive and emotional disorders in post-stroke rats by regulating the TLR-2/NF-κB pathway DOI Creative Commons

Ziqiang Dong,

Zhihui Dong, Lili Xu

et al.

Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 16

Published: March 12, 2025

Cognitive impairments following post-stroke significantly hinder neurological recovery and exacerbate patient morbidity, underscoring urgent need for effective therapeutic strategies. Vortioxetine (VTX), a prominent Selective Serotonin Reuptake Inhibitor (SSRI), boasts notable antidepressant, cognition-enhancing, anti-inflammatory properties. This investigation delves into VTX’s influence on motor skills, spatial learning-memory capabilities, depressive behaviors in Middle Cerebral Artery Occlusion (MCAO) rats, alongside its underlying mechanisms. Our findings reveal that while VTX fails to entirely reverse ischemic-reperfusion damage, it substantially ameliorates spontaneous locomotor functions, augments capacities, exhibits potent antidepressant anxiety-like efficacy. Preliminary data propose these beneficial effects may stem from inflammation modulation via the Toll-Like Receptor 2 (TLR-2)/Nuclear Factor-Kappa B (NF- κ B) signaling pathway. Collectively, our work underscores promising role enhancing motor, cognitive mitigating symptoms cerebrovascular accidents, potentially through regulation. These insights pave way novel interventions addressing complications, warranting further exploration.

Language: Английский

Citations

0
Untargeted metabolomics unveils critical metabolic signatures in novel phenotypes of acute ischemic stroke DOI
Yao Jiang, Qian Wu,

Yingqiang Dang

et al.

Metabolic Brain Disease, Journal Year: 2025, Volume and Issue: 40(3)

Published: Feb. 19, 2025

Language: Английский

Citations

0
Dimethyl phthalate exposure induces cognitive impairment via COX2-mediated neuroinflammation DOI Creative Commons
Haoyuan Yin, Jian Shen,

Xiaoying Qian

et al.

Ecotoxicology and Environmental Safety, Journal Year: 2024, Volume and Issue: 284, P. 117039 - 117039

Published: Sept. 12, 2024

Language: Английский

Citations

2
CLEC7A Knockdown Alleviates Ischemic Stroke by Inhibiting Pyroptosis and Microglia Activation DOI Creative Commons
Wei Li,

Xiaoli Feng,

Manyu Zhang

et al.

Journal of Integrative Neuroscience, Journal Year: 2024, Volume and Issue: 23(12)

Published: Dec. 23, 2024

Background: Ischemic stroke (IS) is the leading cause of mortality worldwide. Herein, we aimed to identify novel biomarkers and explore role C-type lectin domain family 7 member A (CLEC7A) in IS. Methods: Differentially expressed genes (DEGs) were screened using GSE106680, GSE97537, GSE61616 datasets, hub identified through construction protein-protein interaction networks. An IS model was established by middle cerebral artery occlusion reperfusion (MCAO/R). Neural function assessed triphenyl tetrazolium chloride, hematoxylin-eosin, terminal deoxynucleotidyl transferase-mediated nick-end labeling. cell counting kit used detect viability following oxygen-glucose deprivation/reperfusion (OGD/R). Inflammatory factors detected enzyme-linked immunosorbent assay. The mRNA protein expression levels reverse transcription-quantitative polymerase chain reaction western blotting, respectively. Results: Fc fragment Immunoglobulin G (IgG) receptor IIIa (FCGR3A), E (IgE) Ig (FCER1G), Complement component 5a 1 (C5AR1), CLEC7A, Plasminogen activator, urokinase (PLAU), C-C motif chemokine ligand 6 (CCL6) as important genes, from which CLEC7A selected primary subject this study. activation microglia pyroptosis observed MCAO/R with increased interleukin (IL)-1β, IL-18, tumor necrosis factor-α, lactate dehydrogenase. knockdown found promote BV2 cells inhibiting HT22 cells. also decreased infarct volume neurological deficit scores, alleviated injury neuronal apoptosis rats. inhibited microglial model. activator reversed effect on OGD/R-treated Conclusion: a promising biomarker alleviates activation.

Language: Английский

Citations

2
Dimethyl phthalate exposure induces cognitive impairment through COX2-mediated microglial activation DOI Creative Commons
Genghuan Wang, Jian Shen,

Yingcong Lin

et al.

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: March 20, 2024

Abstract AIM We investigated the mechanism of action whereby exposure to dimethyl phthalate (DMP), an environmental pollutant, causes cognitive impairment. METHODS Network pharmacology was used analyze targets and regulatory networks associated with DMP-brain injury-cognitive The intake DMP simulated by exposure, Morris water maze adopted examine tissue levels inflammatory cytokines were detected. Brain damage assayed H&E Nissl staining, protein expression identified Western blotting. effects observed after separate application siRNA-COX2 celecoxib-COX2 inhibitors. In in vitro experiment, on microglia activation investigated. RESULTS revealed that PTGS2 (COX2) significantly correlated DMP, which could act through COX2. After mice showed significant brain injury impairment, along upregulation cytokines. inhibit ameliorate impairment mice. results activate cause neuroinflammation. CONCLUSION can induce neuroinflammation COX2-mediated microglia, resulting COX2 is important target for action.

Language: Английский

Citations

1