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Updated: Jun 23, 2026
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Improved 3D Hydrogel Cultures of Primary Glial Cells for In Vitro Modelling of Neuroinflammation
Published on: December 8, 2017
Biomimetic Hydrogel System Targeting S100A8 Centered Neuroimmune Crosstalk and Hypoxia Induced Neuronal Injury
Peng Liu1, Xiaoyang Wu2, Xiaoyin Liu1
1Department of Neurosurgery, West China Medical School, West China Hospital, Sichuan University, Chengdu, Sichuan, China.
Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|June 22, 2026
Summary
This study introduces HPC@Gel, a novel hydrogel therapy for traumatic brain injury (TBI). It effectively reduces hypoxia and neuroinflammation by targeting S100A8, promoting neural regeneration and recovery.
Area of Science:
- Neuroscience
- Biomaterials Science
- Regenerative Medicine
Background:
- Traumatic brain injury (TBI) involves secondary injury driven by tissue hypoxia and neuroinflammation.
- S100A8, a pro-inflammatory damage-associated molecular pattern, exacerbates TBI by mediating neuron-microglia signaling.
- Current interventions lack effective strategies to target S100A8-centered neuroimmune crosstalk.
Purpose of the Study:
- To develop a multifunctional biomimetic hydrogel system (HPC@Gel) to disrupt the cycle of hypoxia and S100A8-mediated neuroinflammation in TBI.
- To evaluate the neuroprotective and neuroimmune regulatory effects of HPC@Gel in vitro and in vivo.
Main Methods:
- Development of HPC@Gel by integrating modified hemoglobin nanoparticles and curcumin-based carbon quantum dots into a hyaluronic acid-collagen hydrogel.
- In vitro evaluation using hypoxic neurons, LPS-stimulated microglia, and a Transwell model.
- In vivo assessment in a rat cortical cavity TBI model.
Main Results:
- HPC@Gel significantly downregulated S100A8 expression and attenuated neuron-microglia crosstalk in vitro.
- Exogenous S100A8 partially reversed the protective effects of HPC@Gel, confirming its functional role.
- In vivo, HPC@Gel reduced S100A8, alleviated hypoxia, reversed neuroinflammation, promoted neural regeneration, and improved neurological recovery.
Conclusions:
- HPC@Gel demonstrates a promising therapeutic strategy for TBI by simultaneously addressing hypoxia and S100A8-mediated neuroimmune crosstalk.
- This approach facilitates a better pathological microenvironment, enhances endogenous neural repair, and improves functional outcomes after TBI.
