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Dehydrocorydaline Accelerates Palatal Wound Healing in Mice Through Suppression of the p38 MAPK/CCL2 Axis and
Yingyi Chen1, Zhaona Liu1,2, Yijia Wang1
1Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Laboratory of Tissue Regeneration and Immunology, Department of Periodontics, School of Stomatology, Capital Medical University, No. 9 Fanjiacun Road, Beijing 100070, China.
Abstract:
Background/Objectives: Excessive inflammation is a critical contributor to impaired oral mucosal wound healing, yet effective therapeutic strategies are still lacking. Although dehydrocorydaline (DHC) has been reported to exhibit anti-inflammatory and analgesic properties, its role in wound healing and the underlying mechanisms have not been fully elucidated. This study aimed to investigate whether DHC accelerates palatal wound healing and to elucidate the role of the p38 mitogen-activated protein kinase (MAPK)/CCL2 signaling axis in DHC-mediated regulation of macrophage chemotaxis. Methods:In vitro, macrophages were stimulated with 1 μg/mL lipopolysaccharide (LPS) and treated with DHC at 0.1, 1, and 10 μM. The chemotactic response and inflammatory function of macrophages were assessed using real-time PCR, ELISA, Western blotting, and Transwell assays. Molecular docking simulations and Western blotting analyses were performed to examine the regulatory effect of DHC on MAPK signaling pathway. In vivo, a full-thickness palatal mucoperiosteal wound extending from the left maxillary first to third molars was established in mice by scalpel scraping. The effects of topical 10 μM DHC gel on wound healing were evaluated using stereomicroscopy, histological staining, and real-time PCR at 0, 3, and 5 days post-modeling. Results:In vitro, DHC effectively downregulated the expression of chemokines, including C-C motif chemokine ligand 2 (Ccl2), Ccl5, Ccl22, C-X-C motif chemokine ligand 10 (Cxcl10), and Ccl24, with the most significant inhibitory effect on Ccl2 (70.8% inhibition). In Transwell assays, DHC reduced macrophage migration by 68.2%. Mechanistically, DHC prominently inhibited the activation of the MAPK signaling pathway. In vivo, DHC treatment accelerated wound healing and markedly reduced macrophage infiltration in mouse palatal wound tissues. Conclusions: These findings demonstrated that DHC accelerated palatal wound healing 1.6-fold in mice. DHC suppressed macrophage chemotaxis by 68.2% through modulation of the MAPK signaling pathway.
