Protective and therapeutic effects of hexagonal boron nitride against hydrogen peroxide-induced oxidative damage in human gingival fibroblasts

TL;DR

This study explores how hexagonal boron nitride (hBN) can protect human gum cells from oxidative stress caused by hydrogen peroxide.

Contribution

The study introduces hBN as a potential therapeutic agent for periodontal diseases by demonstrating its protective effects against oxidative damage in human gingival fibroblasts.

Findings

hBN improved cell viability in human gingival fibroblasts under oxidative stress.

hBN application did not significantly alter total oxidant status in treated cells.

The protective effects of hBN were modest and not mediated through changes in oxidant levels.

Abstract

Oxidative stress plays a significant role in the progression of periodontal diseases. Hexagonal boron nitride (hBN) nanoparticles have antimicrobial, antiplaque, and antioxidant properties. The aim of this study to evaluate the protective and therapeutic effects of hBN against oxidative stress induced by hydrogen peroxide (H2O2) in human gingival fibroblast (HGF) cells.

In this study, a primary cell line of HGFs was used. Oxidative stress was induced by treating the cells with 800 µM H2O2. hBN was applied at concentrations of 0.001, 0.005, and 0.01 mg/mL, either 2 h prior to or 2 h following H₂O₂ exposure. Cells were incubated for 24 h post-treatment. Cell viability was assessed using the 2,3-bis-[2-methoxy-4-nitro-5-sulfophenyl]-2 H-tetrazolium-5-carboxyanilide salt (XTT) assay. Additionally, the total oxidant status (TOS) was measured before and after oxidative damage at the 0.01 mg/mL hBN concentration.

hBN did not negatively affect cell viability in HGF cells at any concentration. The application of hBN to HGF cells before and after oxidative damage resulted in statistically significant (P < 0.001), albeit modest improvements in cell viability (2-5.5% and 3-6.5%, respectively). No significant differences were observed in TOS (P = 0.234), indicating that the cytoprotective effects were not mediated via alterations in TOS.

Within the limitations of this in vitro study, hBN was found to enhance cell viability under H₂O₂-induced oxidative stress in HGF cells. These findings suggest a potential role for hBN in modulating antioxidant responses and supporting periodontal healing processes. However, their clinical relevance remains uncertain. Therefore, further mechanistic studies and clinical investigations are required to validate the potential adjunctive role of hBN in the prevention and treatment of periodontal diseases.

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