ArticleTranslational neuroscience2025
DIA-based proteomics reveals anti-inflammatory role of DL-3-
Article in Translational neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Cerebral blood flow in conscious rats and implications for therapeutic interventions.Experimental physiology · 2026Review
- A modern reinterpretation of the "kidney governs bone" theory: systemic regulation of the neuro-endocrine-immune network via the brain-bone axis and traditional chinese medicine intervention strategies.Frontiers in pharmacology · 2026Review
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Authors and funding
7 authors.
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Abstract
Objectives: Excessive neuroinflammatory responses represent a key pathological mechanism in cerebral small vessel disease (CSVD). Dl-3- Methods: Forty-week-old spontaneously hypertensive rats were selected as a CSVD rodent model to determine the neuroprotective effects of NBP. Cognitive ability was assessed using the Morris water maze after 28 weeks of treatment. Pathological changes in the brain tissue were observed through immunohistochemistry. Data-independent acquisition (DIA) mass spectrometry was executed to identify the probable targets of NBP in CSVD. Based on the proteomics results, the expression of the toll-like receptor 4 (TLR4)/nuclear factor kappa-B (NF-κB) signaling pathway in the rat hippocampus was evaluated by western blotting and quantitative real-time polymerase chain reaction (qRT-PCR). Results: NBP treatment ameliorated the cognitive abilities and pathological changes in CSVD. DIA proteomics revealed 262 differentially expressed hippocampal proteins, with bioinformatics analysis highlighting acute inflammatory response as a primary target. Furthermore, western blotting and qRT-PCR results confirmed these results and showed that after treatment with NBP, TLR4 regulated NF-κB pathway and inflammatory factors decreased. Conclusions: Our findings demonstrated that NBP exerts neuroprotection in CSVD probably by suppressing TLR4/MyD88/NF-κB-mediated neuroinflammation. This study provides the evidence of NBP's therapeutic mechanisms in CSVD, suggesting its potential as a targeted anti-inflammatory treatment.
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