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Research Snapshot Theater: Sepsis, Adult and Pediatric

Neuroprotective Role of Xijiao Dihuang Decoction in SAE via IL-17 Pathway Modulation

Monday, March 23, 2026
2:30 PM - 3:30 PM Central Time
Location: Connections Central - RST 14
  • ZZ

    Zixuan Zhai, n/a (she/her/hers)

    China (People's Republic)

    Disclosure(s): No relevant financial relationship(s) to disclose.

  • WL

    Wen Li, n/a

    Student
    The Second Hospital of Dalian Medical University

    Disclosure information not submitted.

  • JC

    Jixuan Cui, n/a

    Student
    The Second Hospital of Dalian Medical University

    Disclosure information not submitted.

  • XL

    Xuelu Li, PhD

    Associate Professor
    The Second Hospital of Dalian Medical University, China (People's Republic)

    Disclosure information not submitted.

  • DZ

    Dandan Zhu, PhD

    Associate Professor
    The Second Hospital of Dalian Medical University, China (People's Republic)

    Disclosure information not submitted.

Introduction: Sepsis-associated encephalopathy (SAE) is a diffuse brain dysfunction due to infection, leading to cognitive deficits and high mortality (25–50%). Current treatments are limited to antibiotics and supportive care, lacking specific therapies. Inflammation, BBB disruption, and neuronal apoptosis are key to SAE pathogenesis. Studies show elevated IL-17 in brain microvascular endothelial cells during SAE, suggesting its key role in neural injury. Network pharmacology and molecular docking suggest Xijiao Dihuang Decoction (XDD) may treat SAE via IL-17 pathway modulation, though mechanisms remain unclear.


Methods: SAE- and XDD-related genes were identified using GeneCards, TCMSP, BATMAN, and Venn analysis. A PPI network was built via STRING. GO and KEGG analyses identified IL-17 signaling as a key pathway. Cytoscape identified hub targets. Molecular docking (PyMol, AutoDock) screened active components and targets. An SAE mouse model was established via cecum ligation and puncture (CLP). Mice were grouped into control (sham), model (CLP), and XDD-treated (XDD-CLP). XDD (0.3 mL, 1.875 g/mL crude drug) was administered twice daily for 3 days pre-CLP and once post-CLP. Nissl staining, WB (IBA1, FOS), qPCR (IL-1β, IL-6, TNF-α), brain water content, and Evans Blue assays evaluated therapeutic effects.


Results: A total of 2543 SAE genes and 140 overlapping XDD-SAE targets were identified. KEGG highlighted IL-17 as the key pathway. Five IL-17-related targets (FOS, CHUK, NFKB1, PTGS2, IKBKB) and top hub genes (e.g., PTGS2, NFκB1, TGF-β1) were identified. Docking revealed NFκB1–Cholesterol (−5.7 kcal/mol), NFκB1–Beta-Sitosterol (−5.6 kcal/mol), and PTGS2–Gallic acid (−6.2 kcal/mol) had favorable binding energies.
XDD improved survival in SAE mice and reduced neuronal loss and vacuolation (CA1, CA3, DG). WB showed decreased IBA1 and FOS in XDD-treated mice, indicating reduced microglial activation via IL-17 modulation. qPCR confirmed reduced IL-1β, IL-6, and TNF-α levels. Brain edema and BBB permeability were alleviated, shown by decreased water content and EB extravasation.


Conclusions: XDD exerts neuroprotective effects in SAE by inhibiting neuroinflammation and microglial activation, preserving neurons and BBB integrity, likely through IL-17 pathway regulation, particularly targeting FOS.