Molecular mechanisms of sulforaphane in Alzheimer's disease: insights from an in-silico study.

Autor: Vu GH; Department of Public Heath, Hong Bang Health Center, Hai Phong, Vietnam., Nguyen HD; Department of Pharmacy, College of Pharmacy and Research Institute of Life and Pharmaceutical Sciences, Sunchon National University, Suncheon, 57922 Republic of Korea.
Jazyk: angličtina
Zdroj: In silico pharmacology [In Silico Pharmacol] 2024 Nov 01; Vol. 12 (2), pp. 96. Date of Electronic Publication: 2024 Nov 01 (Print Publication: 2024).
DOI: 10.1007/s40203-024-00267-4
Abstrakt: This study was to identify the molecular pathways that may explain sulforaphane's Alzheimer's disease (AD) benefits using multiple advanced in silico approaches. We found that sulforaphane regulates 45 targets, including TNF, INS, and BCL2. Therefore, it may help treat AD by reducing neuroinflammation, insulin resistance, and apoptosis. The important relationships were co-expression and pathways. 45 targets were linked to the midbrain, metabolite interconversion enzymes, 14q23.3 and 1q31.1 chromosomes, and modified residues. "Amyloid precursor protein catabolic process", "regulation of apoptotic signaling pathway", and "positive regulation of nitric oxide biosynthetic process" were the main pathways, while NFKB1, SP1, RELA, hsa-miR-17-5p, hsa-miR-16-5p, and hsa-miR-26b-5p were transcription factors and miRNAs implicated in sulforaphane In AD treatment, miRNA sponges, dexibuprofen, and sulforaphane may be effective. Furthermore, its unique physicochemical, pharmacokinetic, and biological qualities make sulforaphane an effective AD treatment, including efficient gastrointestinal absorption, drug-like properties, absence of CYP450 enzyme inhibition, not being a substrate for P-glycoprotein, ability to cross the blood-brain barrier, glutathione S-transferase substrate, immunostimulant effects, and antagonistic neurotransmitter effects. Sulforaphane is a promising compound for AD management. Further work is needed to elucidate its therapeutic effects based on our findings, including genes, miRNAs, molecular pathways, and transcription factors.
Supplementary Information: The online version contains supplementary material available at 10.1007/s40203-024-00267-4.
Competing Interests: Conflict of interestThe authors declare no competing interests.
(© The Author(s) 2024.)
Databáze: MEDLINE
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