Investigating the clinical efficacy, safety and molecular mechanism of sulforaphane in autism spectrum disorder: an integrated study combining meta-analysis, network pharmacology, and computational biology
Long J, Liao X, Tang Z, Han K, Chen J, Wang X, Liu J, Zhang Y, Zhang H
BMC pharmacology & toxicology · 1 citation
How it was studied
- Design
- Meta-analysis (indexed by PubMed)
- Studied in
- People
- Main outcome
- Health markers and function
- Intake measured by
- Not stated
Who paid for it
- Funding
- Independent funding
- Nonprofit
- China Disabled Persons’ Federation
- Nonprofit
- China Disabled Persons' Federation
Based on 2 listed funder(s) and full-text disclosure statement.
Publication
- Published
- 2025-11-22 · BMC Pharmacol Toxicol · vol. 26 · issue 1 · p. 217
- Publisher
- BioMed Central
- Cited
- 1 citation · more than 60% of similar papers · 0.3× the field average
- References
- 66 works
- Access
- Open access (journal) · CC-BY-NC-ND
- Research areas
- Genomics, phytochemicals, and oxidative stress · Curcumin's Biomedical Applications · Nuclear Receptors and Signaling
- Keywords
- Autism, Computational model, Autism spectrum disorder, Systems biology, Mechanism (biology), Modelling biological systems
- MeSH
- humans, isothiocyanates, sulfoxides, computational biology, randomized controlled trials as topic, molecular dynamics simulation, molecular docking simulation, autism spectrum disorder, network pharmacology
9 authors
From CN
- Junzi LongCapital Medical University; China Rehabilitation Research Center; Changping Laboratory
- Xingxing LiaoCapital Medical University; China Rehabilitation Research Center; Changping Laboratory
- Zhiqing TangCapital Medical University; China Rehabilitation Research Center
- Kaiyue HanCapital Medical University; China Rehabilitation Research Center
- Jiarou ChenWenzhou Medical University; China Rehabilitation Research Center
- Xianna WangCapital Medical University; China Rehabilitation Research Center
Abstract
Background
Sulforaphane, a natural antioxidant rich in cruciferous vegetables, has emerged as a promising dietary supplement for autism spectrum disorder (ASD). However, its therapeutic efficacy remains controversial, and the pharmacological mechanisms are not fully elucidated.
Methods
Eligible randomized controlled trials were retrieved from PubMed, Web of Science, Embase, and Cochrane Library databases. Review Manager 5.4 was used for meta-analysis and bias risk assessment. Network pharmacology, Mendelian randomization, GEO data analyses, molecular docking, and molecular dynamics simulation were employed to explore the mechanisms of sulforaphane in ASD.
Results
Six trials involving 333 participants were included in the meta-analysis. Pooled results demonstrated that both 4-5 weeks and 8-10 weeks of sulforaphane supplementation significantly decreased the scores on the Social Responsiveness Scale compared to placebo controls. No significant difference was observed in the incidence of adverse events. Network pharmacology identified 10 core targets of sulforaphane in ASD, including AKT1, EGFR, HSP90AA1, SRC, CASP3, STAT1, MAPK1, MMP9, MAPK8, and JAK2. These targets were implicated in the PI3K-Akt signaling pathway, MAPK signaling pathway, Chemokine signaling pathway, Chemical carcinogenesis - reactive oxygen species, TNF signaling pathway, Th17 cell differentiation, mTOR signaling pathway, and IL-17 signaling pathway. Mendelian randomization further revealed an inverse association between STAT1 levels and ASD risk. GEO transcriptomic data provided independent validation for the network pharmacology predictions. The binding energies between sulforaphane and the top 10 core targets are all ≤ -4.0 kcal/mol. Molecular dynamics simulations further validated the stable interaction between MMP-9 and sulforaphane.
Conclusion
Sulforaphane may serve as an efficacious and safe adjunctive therapy for ASD, mediated by its anti-oxidant and anti-inflammatory effects along with the modulation of autophagy.
Prospero registration number
CRD42025635045.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY-NC-ND).
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