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

Yingcong Lin

и другие.

Research Square (Research Square), Год журнала: 2024, Номер unknown

Опубликована: Март 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.

Язык: Английский

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

Xiaoyue Tao,

Yingying Hu,

Niping Mao

и другие.

International Immunopharmacology, Год журнала: 2024, Номер 136, С. 112372 - 112372

Опубликована: Июнь 7, 2024

Язык: Английский

Процитировано

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

и другие.

CNS Neuroscience & Therapeutics, Год журнала: 2024, Номер 30(8)

Опубликована: Авг. 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

Язык: Английский

Процитировано

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

Peng Zhan,

Shiming Huang,

D. Chen

и другие.

Naunyn-Schmiedeberg s Archives of Pharmacology, Год журнала: 2025, Номер unknown

Опубликована: Янв. 2, 2025

Язык: Английский

Процитировано

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

Phytochemistry Reviews, Год журнала: 2025, Номер unknown

Опубликована: Март 11, 2025

Язык: Английский

Процитировано

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

и другие.

Frontiers in Pharmacology, Год журнала: 2025, Номер 16

Опубликована: Март 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.

Язык: Английский

Процитировано

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

Yingqiang Dang

и другие.

Metabolic Brain Disease, Год журнала: 2025, Номер 40(3)

Опубликована: Фев. 19, 2025

Язык: Английский

Процитировано

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

Xiaoying Qian

и другие.

Ecotoxicology and Environmental Safety, Год журнала: 2024, Номер 284, С. 117039 - 117039

Опубликована: Сен. 12, 2024

Язык: Английский

Процитировано

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

Xiaoli Feng,

Manyu Zhang

и другие.

Journal of Integrative Neuroscience, Год журнала: 2024, Номер 23(12)

Опубликована: Дек. 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.

Язык: Английский

Процитировано

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

Yingcong Lin

и другие.

Research Square (Research Square), Год журнала: 2024, Номер unknown

Опубликована: Март 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.

Язык: Английский

Процитировано

1