Salvianolic acid a inhibits neuroinflammation and ameliorates Alzheimer's disease pathology via the p38 MAPK/NF-κB pathway based on network pharmacology and experimental validation.

Λεπτομέρειες βιβλιογραφικής εγγραφής
Τίτλος: Salvianolic acid a inhibits neuroinflammation and ameliorates Alzheimer's disease pathology via the p38 MAPK/NF-κB pathway based on network pharmacology and experimental validation.
Συγγραφείς: Xiao S; Shenzhen Key Laboratory of Marine Biotechnology and Ecology, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen 518060, China; Shenzhen-Hong Kong Institute of Brain Science-Shenzhen Fundamental Research Institutions, Shenzhen 518055, China., Han Y; Shenzhen Key Laboratory of Marine Biotechnology and Ecology, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen 518060, China., Yan J; Shenzhen Key Laboratory of Marine Biotechnology and Ecology, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen 518060, China., Wu L; Shenzhen Key Laboratory of Marine Biotechnology and Ecology, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen 518060, China., Lin H; Shenzhen Key Laboratory of Marine Biotechnology and Ecology, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen 518060, China., Yuan C; Shenzhen Key Laboratory of Marine Biotechnology and Ecology, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen 518060, China., Song C; Shenzhen Key Laboratory of Marine Biotechnology and Ecology, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen 518060, China., Ye J; Shenzhen Key Laboratory of Marine Biotechnology and Ecology, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen 518060, China; Shenzhen-Hong Kong Institute of Brain Science-Shenzhen Fundamental Research Institutions, Shenzhen 518055, China. Electronic address: yejinwang@szu.edu.cn.
Πηγή: International immunopharmacology [Int Immunopharmacol] 2026 Jun 01; Vol. 178, pp. 116594. Date of Electronic Publication: 2026 Apr 01.
Τύπος έκδοσης: Journal Article
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: Elsevier Science Country of Publication: Netherlands NLM ID: 100965259 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1878-1705 (Electronic) Linking ISSN: 15675769 NLM ISO Abbreviation: Int Immunopharmacol Subsets: MEDLINE
Imprint Name(s): Original Publication: Amsterdam ; New York : Elsevier Science, c2001-
Ιατρικοί όροι (MeSH): Alzheimer Disease*/drug therapy , Alzheimer Disease*/pathology , Alzheimer Disease*/metabolism , p38 Mitogen-Activated Protein Kinases*/metabolism , NF-kappa B*/metabolism , Caffeic Acids*/therapeutic use , Caffeic Acids*/pharmacology , Lactates*/therapeutic use , Lactates*/pharmacology , Anti-Inflammatory Agents*/therapeutic use , Anti-Inflammatory Agents*/pharmacology , Neuroinflammatory Diseases*/drug therapy, Signal Transduction/drug effects ; Amyloid beta-Peptides/metabolism ; Cytokines/metabolism ; Animals ; Humans ; Mice ; Network Pharmacology ; Mice, Transgenic ; Disease Models, Animal ; Male ; Cell Line ; Molecular Docking Simulation
Περίληψη: Alzheimer's disease (AD) represents the most prevalent form of neurodegenerative disorder, characterized by progressive cognitive impairments and a scarcity of effective treatments. Salvianolic acid A (SalA), a natural phytochemical endowed with antioxidative, antiapoptotic, and anti-inflammatory properties, emerges as a promising therapeutic candidate for AD. This study explored the therapeutic efficacy and underlying mechanisms of SalA in mitigating AD-related pathologies. Through integrative network pharmacology, molecular docking, and pathway enrichment analysis, p38 MAPK and NF-κB were identified as potential targets of SalA in the context of AD. SalA treatment inhibited the activation of the p38 MAPK/NF-κB pathway via targeting p38 MAPK, leading to decreased levels of IL-1α and IL-1β in lipopolysaccharide (LPS)-stimulated HMC3 cells. In an in vivo 3 × Tg-AD mouse model, SalA administration ameliorated cognitive decline associated with AD, decreased tau protein hyperphosphorylation in the hippocampus and cortex, and reduced amyloid-β (Aβ) accumulation and β-site amyloid precursor protein cleaving enzyme 1 (BACE1) levels. Furthermore, SalA attenuated the activation of the p38 MAPK/NF-κB pathway and the expression of related inflammatory cytokines in the brains of 3 × Tg-AD mice. In conclusion, this study elucidates the promising ameliorative effects of SalA on improving AD pathology, primarily through the modulation of the p38 MAPK/NF-κB signaling pathway.
(Copyright © 2026 Elsevier B.V. All rights reserved.)
Contributed Indexing: Keywords: Alzheimer's disease; NF-κB; Network pharmacology; Salvianolic acid a; p38 MAPK
Substance Nomenclature: 51622542XO (salvianolic acid A)
EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
0 (NF-kappa B)
0 (Caffeic Acids)
0 (Lactates)
0 (Anti-Inflammatory Agents)
0 (Amyloid beta-Peptides)
0 (Cytokines)
Entry Date(s): Date Created: 20260403 Date Completed: 20260714 Latest Revision: 20260714
Update Code: 20260714
DOI: 10.1016/j.intimp.2026.116594
PMID: 41930874
Βάση Δεδομένων: MEDLINE