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Updated: Jun 28, 2025

Organotypic Tissue Model Systems for Investigating Host-Pathogen Interactions In Vitro
Published on: March 28, 2025
Effects of grape seed proanthocyanidins on the expression of inflammatory mediators in gingival epithelial cells
Xiujuan Zhang1, Wei Wu1, Xin Chen1
1The Affiliated Stomatological Hospital of Nanchang University, Key Laboratory of Oral Biomedicine of Jiangxi Province, Nanchang 330006, China.
Objectives:
This study aims to determine the effect of grape seed proanthocyanidin (GSP) pretreatment on lipopolysaccharide (LPS)-induced inflammation of human gingival epithelial cells (HGECs).
Methods:
HGECs were cultivated with different concentrations of GSPs (0, 1, 5, 10, 20, 40, 60, 80, 100 μg·mL-1) for 6, 12, 24, and 48 h. CCK-8 was used to detect the proliferation activity of HGECs. HGECs were treated with different concentrations of GSPs (0, 10, 20, and 40 μg·mL-1) for 24 h and then cultured with 1.0 μg·mL-1 LPS. Enzyme-linked immunosorbent assay (ELISA) was used to detect the expression levels of pro-inflammatory cytokine tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, and IL-6 and anti-inflammatory cytokines IL-4, IL-10, and transforming growth factor-β (TGF-β). Quantitative real-time polymerase chain reaction (QRT-PCR) was used to detect the mRNA expression levels of TNF-α, IL-1β, IL-6, IL-4, IL-10, and TGF-β.
Results:
When the GSP concentration was 0-40 μg·mL-1, the cell proliferation had no significant difference. When the action time reached 24 h, the cell proliferation was the highest. The results of ELISA and QRT-PCR showed that 10, 20, and 40 μg·mL-1 GSPS decreased the expression levels of TNF-α, IL-1β, and IL-6 (P<0.05) and increased the expression levels of IL-4, IL-10, and TGF-β compared with 0 μg·mL-1 GSPS (P<0.05).
Conclusions:
GSPS (0-40 μg·mL-1) has no significant effect on the proliferation activity of HGECs. Pretreatment with GSPS can inhibit the expression of pro-inflammatory factors and enhance the expression of anti-inflammatory factors. Hence, GSPS has a certain preventive effect on the resistance of HGECs to the stimulation of endotoxin.

