Graduate Program in Pediatric Dentistry, Faculty of Dentistry, Chulalongkorn University, Bangkok, 10330, Thailand.
Banphue Hospital, 134 Moo 2, Plubphue Road, Banphue District, Udonthani, 41160, Thailand.
BMC Oral Health. 2021 Oct 17;21(1):535. doi: 10.1186/s12903-021-01890-9.
Curcumin accelerates healing of oral wounds; however, the responsible mechanisms remain underexplored. Our hypothesis is curcumin regulates the expression of wound healing-related genes in human gingival fibroblasts (hGFs). This study investigated whether curcumin regulates transforming growth factor (TGF)-β1, type I TGF-β receptor (TGF-βRI), type II TGF-β receptor (TGF-βRII), and vascular endothelial growth factor (VEGF) expression in unwounded hGFs and an in vitro hGF wound healing model.
The cytotoxicity of curcumin was evaluated using the MTT assay. Unwounded hGFs were treated with non-cytotoxic concentrations of curcumin for 24 h. Gene expression was determined by quantitative polymerase chain reaction. Then, hGFs were treated with 1 µM curcumin in an in vitro wound healing model. PD98059 pretreatment was performed to determine whether extracellular signal-regulated kinase (ERK) signaling was required for regulation of gene expression by curcumin.
Curcumin at 0.1-20 µM caused no significant change in cell viability. In unwounded hGFs, curcumin had no significant effect on TGF-β1, TGF-βRI, TGF-βRII, or VEGF expression. Conversely, curcumin significantly upregulated the expression of these genes in the in vitro wound healing model. PD98059 significantly attenuated the curcumin-stimulated TGF-βRI, TGF-βRII, and VEGF expression, whereas it had no effect on TGF-β1 expression.
Curcumin upregulated TGF-β1, TGF-βRI, TGF-βRII, and VEGF expression in an in vitro hGF wound healing model. The ERK pathway is required for TGF-βRI, TGF-βRII, and VEGF induction by curcumin. Our findings support the development of curcumin as a therapeutic agent for gingival ulcers.
姜黄素能加速口腔伤口愈合；然而，其作用机制仍有待深入研究。我们的假设是姜黄素能调节人牙龈成纤维细胞（hGFs）中与伤口愈合相关的基因表达。本研究旨在探讨姜黄素是否能调节未受伤的 hGFs 中转化生长因子（TGF）-β1、TGF-β 受体Ⅰ（TGF-βRI）、TGF-β 受体Ⅱ（TGF-βRII）和血管内皮生长因子（VEGF）的表达，并在体外 hGF 伤口愈合模型中进行验证。
采用 MTT 法评估姜黄素的细胞毒性。用无细胞毒性浓度的姜黄素处理未受伤的 hGFs 24 小时。采用实时定量聚合酶链反应（PCR）检测基因表达。然后，在体外伤口愈合模型中用 1μM 姜黄素处理 hGFs。用 PD98059 预处理以确定 ERK 信号通路是否是姜黄素调节基因表达所必需的。
0.1-20μM 的姜黄素对细胞活力无显著影响。在未受伤的 hGFs 中，姜黄素对 TGF-β1、TGF-βRI、TGF-βRII 或 VEGF 的表达没有显著影响。相反，姜黄素在体外伤口愈合模型中显著上调了这些基因的表达。PD98059 显著减弱了姜黄素刺激的 TGF-βRI、TGF-βRII 和 VEGF 表达，但对 TGF-β1 表达无影响。
姜黄素能上调体外 hGF 伤口愈合模型中 TGF-β1、TGF-βRI、TGF-βRII 和 VEGF 的表达。ERK 通路是姜黄素诱导 TGF-βRI、TGF-βRII 和 VEGF 表达所必需的。我们的研究结果支持将姜黄素开发为治疗牙龈溃疡的药物。
