Journal of integrative neuroscience · 2026
Atractylodin Suppresses Fibrotic Scar Formation and Enhances Functional Recovery Following Spinal Cord Injury.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Li Zhenwei, Fang Chao, Feng Chengcheng, Wu Zuomeng, Zhao Chenhao, Shen Cailiang
Аннотация
BACKGROUND: Fibrous scar formation significantly inhibits axonal regeneration and functional recovery following spinal cord injury (SCI). Atractylodin (ATD), an active constituent of traditional Chinese medicine, exhibits broad pharmacological properties, including anti-inflammatory and anti-fibrotic effects. Nevertheless, the potential therapeutic role of ATD in SCI and its underlying molecular mechanisms remain to be fully elucidated.
METHODS: An SCI model was established in C57 mice. Motor function was assessed using the Basso Mouse Scale scoring system, inclined plane test, swimming test, and footprint analysis. Immunohistochemical staining was performed to evaluate fibrotic scar formation and neuronal survival. Western blotting and quantitative real-time PCR (qPCR) were also employed to investigate the molecular mechanisms underlying ATD-mediated regulation of fibroblasts following SCI.
RESULTS: ATD administration significantly enhanced motor function in SCI mice, reduced the area of fibrotic scars, and suppressed the expression of fibrotic markers. Mechanistically, ATD inhibited Mothers Against Decapentaplegic Homolog 2/3 (SMAD2/3) phosphorylation and nuclear translocation, thereby suppressing fibroblast activation and extracellular matrix deposition, while promoting neuronal survival and axonal regeneration.
CONCLUSIONS: ATD mitigates fibrotic scar formation by targeting the Transforming Growth Factor Beta (TGF-β)/SMAD pathway, thereby facilitating axonal regeneration and functional recovery. This offers a promising therapeutic strategy for SCI.
METHODS: An SCI model was established in C57 mice. Motor function was assessed using the Basso Mouse Scale scoring system, inclined plane test, swimming test, and footprint analysis. Immunohistochemical staining was performed to evaluate fibrotic scar formation and neuronal survival. Western blotting and quantitative real-time PCR (qPCR) were also employed to investigate the molecular mechanisms underlying ATD-mediated regulation of fibroblasts following SCI.
RESULTS: ATD administration significantly enhanced motor function in SCI mice, reduced the area of fibrotic scars, and suppressed the expression of fibrotic markers. Mechanistically, ATD inhibited Mothers Against Decapentaplegic Homolog 2/3 (SMAD2/3) phosphorylation and nuclear translocation, thereby suppressing fibroblast activation and extracellular matrix deposition, while promoting neuronal survival and axonal regeneration.
CONCLUSIONS: ATD mitigates fibrotic scar formation by targeting the Transforming Growth Factor Beta (TGF-β)/SMAD pathway, thereby facilitating axonal regeneration and functional recovery. This offers a promising therapeutic strategy for SCI.