Ascorbic Acid's Effect On Inflamed Dental Pulp Microenvironment

This study investigates the effects of ascorbic acid on inflammatory cytokines produced by dental pulp cells in vitro and the pathological progression of pulp tissue inflammation in vivo, within a lipopolysaccharide (LPS)-induced inflammatory microenvironment. Human dental pulp cells (HDPCs) were stimulated with 1 μg/ml LPS in vitro to induce an inflammatory microenvironment, followed by intervention with 50 μM ascorbic acid. Cell proliferation was assessed using the MTT assay, and the expression levels of IL-6, IL-8, and IL-10 were measured via ELISA. For the in vivo study, a rat pulpitis model was established by applying 1 mg/mL LPS to exposed pulp tissue. The experimental group received topical 50 μM ascorbic acid, while the control group received normal saline. Rats were euthanized after 2 days. Hematoxylin-eosin (HE) staining and immunohistochemistry were used to evaluate histopathological changes and the levels of IL-6, IL-8, and IL-10 in the pulp tissue. In the LPS-induced inflammatory microenvironment, 50 μM ascorbic acid significantly promoted HDPC proliferation, while markedly reducing the production of IL-6 and IL-8 and increasing IL-10. The in vivo rat study also demonstrated that ascorbic acid reduced inflammatory cell infiltration in the dental pulp. In an LPS-induced inflammatory microenvironment, 50 μM ascorbic acid promotes the proliferation of dental pulp cells. Early supplementation with ascorbic acid reduces the levels of pro-inflammatory cytokines (IL-6, IL-8), increases the anti-inflammatory cytokine IL-10, and alleviates pulp inflammation.