Kaokai Taweesak, Ittichaicharoen Jitjiroj, Srisuwan Tanida
Dental Department, Phobphra Hospital, Tak, Thailand.
Department of Oral Medicine and Diagnostic Science, Chiang Mai University, Chiang Mai, Thailand.
J Dent Sci. 2025 Jul;20(3):1546-1553. doi: 10.1016/j.jds.2024.12.007. Epub 2024 Dec 16.
BACKGROUND/PURPOSE: Effective dental pulp healing is essential for preserving tooth vitality. Although beta-glucan has shown promise in wound healing in the medical fields, its potential effects on human dental pulp cells (HDPCs) remain unexplored. This study aimed to assess beta-glucan's effects on HDPC proliferation, migration, collagen synthesis, mineralization, and differentiation.
Primary HDPCs were cultured and assigned into five groups: control, vehicle, and beta-glucan at concentrations of 5, 7.5, and 10 mg/mL. Cell proliferation was quantified using the alamarBlue® assay at 24, 48, and 72 h. Cell migration was assessed at 12 and 24 h via the scratch wound healing assay. Flow cytometry was employed to detect integrin beta 1 (CD29) expression during wound healing. Mineralization and differentiation at day 14 were evaluated through alizarin red S staining and quantitative real-time polymerase chain reaction (qRT-PCR), measuring Dentin Sialophosphoprotein (DSPP), Interleukin-10 (IL-10), and Collagen type I (COL1) gene expression. Statistical significance was established at < 0.05.
At 24 and 72 h, all concentrations of beta-glucan significantly induced cell proliferation. In the wound healing assay, beta-glucan improved cell migration and increased the expression of integrin beta 1 after 24 h. Mineralized matrix formation and the expression of IL-10 and COL1 were significantly observed at 14 days. The upregulation of DSPP was detected in groups supplemented with 5 and 7.5 mg/mL beta-glucan.
Beta-glucan enhanced cell proliferation, cell migration potential, integrin beta 1 expression, mineralized matrix formation, and DSPP, IL-10, and COL1 gene expression in HDPCs.
背景/目的：有效的牙髓愈合对于维持牙齿活力至关重要。尽管β-葡聚糖在医学领域的伤口愈合中已显示出前景，但其对人牙髓细胞（HDPCs）的潜在影响仍未得到探索。本研究旨在评估β-葡聚糖对HDPCs增殖、迁移、胶原合成、矿化和分化的影响。
培养原代HDPCs并分为五组：对照组、赋形剂组以及浓度为5、7.5和10mg/mL的β-葡聚糖组。在24、48和72小时使用alamarBlue® 检测法定量细胞增殖。在12和24小时通过划痕伤口愈合试验评估细胞迁移。采用流式细胞术检测伤口愈合过程中整合素β1（CD29）的表达。在第14天通过茜素红S染色和定量实时聚合酶链反应（qRT-PCR）评估矿化和分化，测量牙本质涎磷蛋白（DSPP）、白细胞介素-10（IL-10）和I型胶原（COL1）基因表达。以P < 0.05确定统计学显著性。
在24和72小时，所有浓度的β-葡聚糖均显著诱导细胞增殖。在伤口愈合试验中，β-葡聚糖改善了细胞迁移并在24小时后增加了整合素β1的表达。在第14天观察到明显的矿化基质形成以及IL-10和COL1的表达。在补充有5和7.5mg/mLβ-葡聚糖的组中检测到DSPP的上调。
β-葡聚糖增强了HDPCs的细胞增殖、细胞迁移潜能、整合素β1表达、矿化基质形成以及DSPP、IL-10和COL1基因表达。
