Essential Oils from Ugandan Medicinal Plants: In Vitro Cytotoxicity and Effects on IL-1 β-Induced Proinflammatory Mediators by Human Gingival Fibroblasts

Abstract

The study investigated cytotoxicity of essential oils from four medicinal plants (Bidens pilosa, Ocimum gratissimum, Cymbopogon nardus, and Zanthoxylum chalybeum) on human gingival fibroblasts and their effects on proinflammatory mediators' secretion. Cytotoxicity of essential oils was investigated using 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay. Effects of essential oils at subcytotoxicity concentrations on interleukin- (IL-) 6, IL-8, and prostaglandin E₂ (PGE₂) secretions by gingival fibroblasts treated with IL-1β (300 pg/mL) were evaluated by ELISA and EIA. IC₅₀ values of the essential oils ranged from 26 μg/mL to 50 μg/mL. Baseline and IL-1β-induced secretion of PGE₂ was inhibited by treatment with essential oil from O. gratissimum. Essential oils from B. pilosa and C. nardus had synergistic effects with IL-1β on PGE₂ seceretion. In conclusion, the study suggests that essential oil from O. gratissimum decreases gingival fibroblasts secretion of PGE₂, while essential oils from B. pilosa and C. nardus increase PGE₂ secretion. Essential oil from Z. chalybeum was the most cytotoxic, while oil from C. nardus was the least cytotoxic. Although the clinical significance of these findings remains to be determined, it may be suggested that essential oil from O. gratissimum, applied at subcytotoxicity concentrations, could reduce the participation of gingival fibroblasts in the gingival inflammation and tissue destruction associated with periodontitis.

Figure 1

Effects of essential oils from Ugandan medicinal plants on IL-1β-induced IL-6, IL-8, and PGE₂ in human gingival fibroblasts. Human gingival fibroblasts were treated with IL-1β alone (300 pg/mL), essential oils at increasing subcytotoxicity concentrations, or combination of IL-1β (300 pg/mL) and essential oils. Untreated cells were used as control. IL-6 and IL-8 were assessed by enzyme-linked immunosorbent assay (ELISA). PGE₂ was assessed by enzyme immunoassay (EIA). The data are the means ± standard deviations of triplicate assays for three independent experiments. Statistical significance was determined using one-way ANOVA and Tukey's post hoc test. ^∗ P < 0.05 compared with the untreated control; ^# P < 0.05 compared with cells stimulated with 300 pg/mL IL-β alone.