Related Experiment Video
Updated: Jun 1, 2025
Author Spotlight: Exploring Photodynamic Therapy with Curcumin in a Murine Model for Oral Candidiasis
Published on: October 27, 2023
Curcumin pretreatment prevents butyrate-induced cell death and release of damage-associated molecular patterns on
Takayuki Hirasawa1, Kiwa Miyake2, Keiji Shinozuka2
1Division of Oral Structural and Functional Biology, Nihon University Graduate School of Dentistry, Tokyo, Japan; Department of Oral and Maxillofacial Surgery II, Nihon University School of Dentistry, Tokyo, Japan.
Objectives:
Exposure of gingival epithelial cells to butyrate, a short-chain fatty acid produced by dental plaque bacteria, cause cell death and subsequent damage-associated molecular pattern (DAMP) release. We investigated the effects of curcumin, a polyphenol extracted from turmeric, on butyrate-induced human gingival epithelial Ca9-22 cell death and DAMP release.
Methods:
Ca9-22 cells were pretreated with curcumin before butyrate exposure. Cell death was quantified using SYTOX green dye, and histone H3 acetylation was analyzed by Western blot. Conditioned media were collected to detect DAMPs by Western blot. We also assessed the effects of the histone acetyltransferase (HAT) inhibitor C646, instead of curcumin, on butyrate-induced cell death, DAMP release, and histone H3 acetylation, and examined the effects of curcumin pretreatment on cell death, DAMP release, and histone H3 acetylation induced by the histone deacetylase (HDAC) inhibitors, valproate and suberoylanilide hydroxamic acid (SAHA).
Results:
Curcumin pretreatment attenuated butyrate-induced Ca9-22 cell death, histone H3 acetylation, and release of the DAMPs. The C646 also attenuated butyrate-induced cell death, DAMP release, and histone H3 acetylation. Curcumin also suppressed cell death, DAMP release, and histone H3 acetylation triggered by the HDAC inhibitors (valproate and SAHA).
Conclusions:
Curcumin pretreatment ameliorated butyrate-induced histone H3 acetylation, cell death, and DAMP release. As elevated histone acetylation by HDAC inhibitors correlates with increased cell death, while reduced acetylation by a HAT inhibitor is associated with their attenuation, protective effects of curcumin against butyrate-induced Ca9-22 cell death and subsequent DAMP release may occur via suppression of histone acetylation.
