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<p>The objective of this study is to evaluate the cytotoxic and inflammatory responses of adult human dermal fibroblasts (hDFs) to HEMA, with and without resveratrol (RSV). hDFs were exposed for 24&#xa0;h to HEMA (4, 8, and 16 mM) in DMEM with and without RSV. Cell viability was assessed by MTT, cell death type was quantified by annexin V-FITC/PI flow cytometry. The expression levels of the IL-8, IL-10, and BCL-2 genes were evaluated using RT-qPCR. Scratch closure was evaluated by the scratch assay. Statistical analysis was conducted using one-way ANOVA, Tukey’s post hoc test, and independent-samples t-test (<i>p</i> &lt; 0.05). HEMA induced a dose-dependent cytotoxic effect in hDFs, with reduced viability at 4–16 mM (<i>p</i> &lt; 0.05), and the highest rate of cell death at 16 mM. Annexin V/PI staining showed increased late apoptosis/necrosis, while RSV co-treatment improved cell survival and reduced apoptotic cell percentages. HEMA upregulated IL-8 expression in a concentration-dependent manner, reaching statistical significance at 4 and 8 mM (<i>p</i> &lt; 0.05), with a markedly elevated but non-significant increase observed at 16 mM (~ 214-fold, <i>p</i> = 0.078). RSV co-treatment restored IL-8 levels to values comparable to the control group across all HEMA concentrations tested (<i>p</i> &gt; 0.05). RSV also enhanced IL-10 expression (~ 614-fold, <i>p</i> = 0.002). This pronounced fold-change is largely attributable to the very low basal IL-10 expression in untreated fibroblasts. In the scratch assay, RSV co-treatment promoted scratch closure, with near-complete closure observed in the 4 mM HEMA + RSV group at 20&#xa0;h. BCL-2 gene expression levels in all experimental groups did not show statistically significant differences compared with the control group (<i>p</i> &gt; 0.05). HEMA demonstrated dose-dependent cytotoxic and pro-inflammatory effects on hDFs, while RSV exhibited protective properties by enhancing cell viability, reducing apoptotic and necrotic cell percentages, attenuating pro-inflammatory IL-8 expression, and promoting scratch closure. These findings suggest that in this in vitro surrogate oxidative-stress model, RSV may mitigate HEMA-induced adverse cellular responses; direct dental or clinical relevance remains indirect and requires confirmation in oral tissue-derived cells. RSV shows promising potential to attenuate HEMA-induced cytotoxic and inflammatory effects in vitro, and may support soft-tissue healing. However, these findings are preliminary and further studies, including investigations in oral tissue-derived cells and protein-level validation, are needed before clinical inferences can be drawn.</p>

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Role of resveratrol in protection against HEMA-induced gene expression level in cell culture

  • 期刊论文

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  • 发表日期：

    2026年8月3日

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  • Neslihan Celik,
  • Merve Iscan Yapar,
  • Kemal Alp Nalcı,
  • Ahmet Hacımuftuoglu

摘要

The objective of this study is to evaluate the cytotoxic and inflammatory responses of adult human dermal fibroblasts (hDFs) to HEMA, with and without resveratrol (RSV). hDFs were exposed for 24 h to HEMA (4, 8, and 16 mM) in DMEM with and without RSV. Cell viability was assessed by MTT, cell death type was quantified by annexin V-FITC/PI flow cytometry. The expression levels of the IL-8, IL-10, and BCL-2 genes were evaluated using RT-qPCR. Scratch closure was evaluated by the scratch assay. Statistical analysis was conducted using one-way ANOVA, Tukey’s post hoc test, and independent-samples t-test (p < 0.05). HEMA induced a dose-dependent cytotoxic effect in hDFs, with reduced viability at 4–16 mM (p < 0.05), and the highest rate of cell death at 16 mM. Annexin V/PI staining showed increased late apoptosis/necrosis, while RSV co-treatment improved cell survival and reduced apoptotic cell percentages. HEMA upregulated IL-8 expression in a concentration-dependent manner, reaching statistical significance at 4 and 8 mM (p < 0.05), with a markedly elevated but non-significant increase observed at 16 mM (~ 214-fold, p = 0.078). RSV co-treatment restored IL-8 levels to values comparable to the control group across all HEMA concentrations tested (p > 0.05). RSV also enhanced IL-10 expression (~ 614-fold, p = 0.002). This pronounced fold-change is largely attributable to the very low basal IL-10 expression in untreated fibroblasts. In the scratch assay, RSV co-treatment promoted scratch closure, with near-complete closure observed in the 4 mM HEMA + RSV group at 20 h. BCL-2 gene expression levels in all experimental groups did not show statistically significant differences compared with the control group (p > 0.05). HEMA demonstrated dose-dependent cytotoxic and pro-inflammatory effects on hDFs, while RSV exhibited protective properties by enhancing cell viability, reducing apoptotic and necrotic cell percentages, attenuating pro-inflammatory IL-8 expression, and promoting scratch closure. These findings suggest that in this in vitro surrogate oxidative-stress model, RSV may mitigate HEMA-induced adverse cellular responses; direct dental or clinical relevance remains indirect and requires confirmation in oral tissue-derived cells. RSV shows promising potential to attenuate HEMA-induced cytotoxic and inflammatory effects in vitro, and may support soft-tissue healing. However, these findings are preliminary and further studies, including investigations in oral tissue-derived cells and protein-level validation, are needed before clinical inferences can be drawn.