ArticleJournal of orthopaedic surgery and research2026
Clec7a-targeted Res@GelMA hydrogels regulate macrophage polarization to reduce neuroinflammation and promote spinal cord repair.
Article in Journal of orthopaedic surgery and research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Excessive inflammation driven by macrophage phenotype imbalance is a key pathological barrier hindering neural repair after spinal cord injury (SCI). Here, methacryloyl gelatin hydrogel (GelMA) loaded with natural anti-inflammatory agent resveratrol (Res) was designed and synthesized. Scanning electron microscopy (SEM), x-ray diffraction (XRD), fourier-transform infrared spectroscopy (FT-IR), Ultraviolet (UV) and rheological characterization confirmed that Res-loaded GelMA hydrogel (Res@GelMA) was successfully synthesized. High-Performance Liquid Chromatography (HPLC) analysis demonstrated sustained Res release. CCK8 and cell adhesion experiments confirmed that Res@GelMA treatment did not affect the cell function of RAW264.7 and had good cell compatibility. Flow cytometry, Enzyme-Linked Immunosorbent Assay (ELISA) and western blot assays revealed that Res@GelMA treatment promoted RAW264.7 to M2 polarization, while reducing the levels of inflammatory factors (IL-1β, IL-6, TNF-α) and down-regulating the expression of IL-1R1/MyD88/TNFR1 inflammatory signaling proteins. Transcriptome sequencing combined with functional screening identified C-type lectin receptor Clec7a as a key target gene regulated by Res@GelMA. Importantly, knockdown of Clec7a and Res@GelMA were both anti-inflammatory, promoted M2 polarization, and blocked the activation of the TLR2/TLR4-p38 MAPK signaling axis. In the SCI mouse model, local implantation of Res@GelMA significantly improved tissue pathological damage and enhanced motor function recovery compared with free Res or blank GelMA. In addition, Res@GelMA achieved systemic anti-inflammation by downregulating the Clec7a-TLR-p38 pathway in the injured area and promoting M2 polarization. This study developed an anti-inflammatory hydrogel material that can regulate the phenotype of macrophages, laying a theoretical and technical foundation for the development of neural repair strategies targeting the inflammatory microenvironment.
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