Archives of oral biology · 2026
Standardized Centella asiatica extract (ECa 233) mitigates chlorhexidine-induced cytotoxicity and promotes oral wound repair via immunomodulation and angiogenesis.
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Rotpenpian Nattapon, Puengsurin Duangchewan, Arayapisit Tawepong, Surarit Rudee, Tantisira Mayuree H, Wanasuntronwong Aree
Аннотация
OBJECTIVE: Although 0.12% Chlorhexidine (CHX) is the gold standard oral antiseptic, its significant cytotoxicity often delays tissue repair. This study investigated the potential of ECa 233, a standardized Centella asiatica extract, to mitigate CHX-induced damage and promote oral wound regeneration.
DESIGNS: Antimicrobial efficacy was assessed via minimum inhibitory concentration (MIC) against key oral pathogens. Human Gingival Fibroblasts (HGFs) were treated with CHX and ECa 233 to evaluate viability (MTT) and migration (scratch assay). Anti-inflammatory effects were measured by quantifying CD80 expression and cytokine secretion (TNF-alpha, IL-6) in LPS-stimulated U937 cells, while angiogenesis was evaluated using the chick embryo chorioallantoic membrane (CAM) assay.
RESULTS: Results demonstrated that ECa 233 preserved the antimicrobial activity of CHX. While 0.12% CHX alone significantly inhibited HGF viability and migration (p < 0.001), the addition of 0.05% ECa 233 significantly rescued these cellular parameters (p < 0.05). ECa 233 effectively downregulated the M1 macrophage marker CD80 and suppressed the secretion of TNF-alpha and IL-6, indicating potent immunomodulatory activity. Furthermore, ECa 233 significantly enhanced vascular density and branching complexity in the CAM assay (p < 0.005).
CONCLUSION: The ECa 233-CHX formulation maintains essential antimicrobial efficacy while reducing cytotoxicity and actively promoting fibroblast migration, immunomodulation, and angiogenesis. This dual-action approach addresses the clinical limitation of antiseptic-induced tissue toxicity, offering a superior biological strategy for enhancing oral wound healing and post-surgical recovery.
DESIGNS: Antimicrobial efficacy was assessed via minimum inhibitory concentration (MIC) against key oral pathogens. Human Gingival Fibroblasts (HGFs) were treated with CHX and ECa 233 to evaluate viability (MTT) and migration (scratch assay). Anti-inflammatory effects were measured by quantifying CD80 expression and cytokine secretion (TNF-alpha, IL-6) in LPS-stimulated U937 cells, while angiogenesis was evaluated using the chick embryo chorioallantoic membrane (CAM) assay.
RESULTS: Results demonstrated that ECa 233 preserved the antimicrobial activity of CHX. While 0.12% CHX alone significantly inhibited HGF viability and migration (p < 0.001), the addition of 0.05% ECa 233 significantly rescued these cellular parameters (p < 0.05). ECa 233 effectively downregulated the M1 macrophage marker CD80 and suppressed the secretion of TNF-alpha and IL-6, indicating potent immunomodulatory activity. Furthermore, ECa 233 significantly enhanced vascular density and branching complexity in the CAM assay (p < 0.005).
CONCLUSION: The ECa 233-CHX formulation maintains essential antimicrobial efficacy while reducing cytotoxicity and actively promoting fibroblast migration, immunomodulation, and angiogenesis. This dual-action approach addresses the clinical limitation of antiseptic-induced tissue toxicity, offering a superior biological strategy for enhancing oral wound healing and post-surgical recovery.