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Background <p>Severe periodontitis has impacted upwards of 1&#xa0;billion people worldwide, posing a public health challenge. <i>Porphyromonas gingivalis</i> (<i>P. gingivalis</i>) is a keystone pathogen implicated in periodontal dysbiosis and disease progression. Lemongrass essential oil (LEO), extracted from <i>Cymbopogon citratus</i> (DC.) Stapf, has shown clinical benefits in periodontitis management, yet its mechanisms remain poorly understood.</p> Methods <p>Antibacterial and bactericidal activities of LEO against <i>P. gingivalis</i> were evaluated, along with its effects on heme uptake and storage, early biofilm-related phenotypes, mature biofilm development, and transcriptional regulation of virulence-associated genes. Docking simulations were performed to predict interactions between metabolites identified via GC-MS and virulence-related proteins. LEO’s effects on oxidative stress, inflammatory cytokine secretion, and ferroptosis-related gene expression were also evaluated in LPS-induced RAW 264.7 macrophages.</p> Results <p>The antibacterial efficacy of LEO against <i>P. gingivalis</i> was evidenced by a 51.10 ± 2.17&#xa0;mm inhibition zone, along with minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) values of 34.06 and 68.13&#xa0;µg/mL, respectively. Growth curve analysis showed sustained suppression over 30&#xa0;h. At 1/4 − 1/2 MIC, LEO inhibited <i>P. gingivalis</i> hemagglutination, hemolysis (<i>p</i> &lt; 0.05), and heme accumulation. Moreover, biofilm formation was significantly reduced by over 85% at 1/2 MIC though suppression of autoaggregation and hydrophobicity (<i>p</i> &lt; 0.05). Molecular docking analysis predicted that <i>α</i>-citral (46.41%) and neral (31.58%), the major metabolites of LEO, may act as potential bioactive metabolites. In addition, LEO significantly reduced the levels of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6), notably decreasing TNF-α secretion to 0.82× and 0.66× (MIC and MBC, respectively) relative to the LPS group (<i>p</i> &lt; 0.05). It also alleviated oxidative stress through <i>slc7a11</i> upregulation and subsequent glutathione synthesis, leading to restoration of the GSH/GSSG ratio and a reduction in ROS and MDA levels (<i>p</i> &lt; 0.05). Moreover, LEO downregulated <i>Tfrc</i> expression and decreased Fe²⁺ accumulation (<i>p</i> &lt; 0.05), suggesting its potential role in restoring iron homeostasis and suppressing ferroptosis-associated markers, such as <i>Ptgs2</i>. These effects highlight the multifunctional regulatory capacity of LEO during <i>P. gingivalis</i>-LPS-induced inflammatory stress.</p> Conclusion <p>LEO demonstrated multitarget inhibitory effects by attenuating <i>P. gingivalis</i> virulence and regulating macrophage oxidative and iron homeostasis. These findings support its potential as a natural adjunctive or preventive agent in periodontitis therapy.</p>

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Multitarget inhibitory effects of lemongrass essential oil on Porphyromonas gingivalis: synergistic regulation of heme utilization, biofilm formation, and the metabolic pathway of ferroptosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月7日

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  • Yue Yuan,
  • Jinlong Sun ,
  • Rifat Nowshin Raka,
  • Zixuan Liu,
  • Zhongwei Zhang ,
  • Junsong Xiao,
  • Hua Wu

摘要

Background

Severe periodontitis has impacted upwards of 1 billion people worldwide, posing a public health challenge. Porphyromonas gingivalis (P. gingivalis) is a keystone pathogen implicated in periodontal dysbiosis and disease progression. Lemongrass essential oil (LEO), extracted from Cymbopogon citratus (DC.) Stapf, has shown clinical benefits in periodontitis management, yet its mechanisms remain poorly understood.

Methods

Antibacterial and bactericidal activities of LEO against P. gingivalis were evaluated, along with its effects on heme uptake and storage, early biofilm-related phenotypes, mature biofilm development, and transcriptional regulation of virulence-associated genes. Docking simulations were performed to predict interactions between metabolites identified via GC-MS and virulence-related proteins. LEO’s effects on oxidative stress, inflammatory cytokine secretion, and ferroptosis-related gene expression were also evaluated in LPS-induced RAW 264.7 macrophages.

Results

The antibacterial efficacy of LEO against P. gingivalis was evidenced by a 51.10 ± 2.17 mm inhibition zone, along with minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) values of 34.06 and 68.13 µg/mL, respectively. Growth curve analysis showed sustained suppression over 30 h. At 1/4 − 1/2 MIC, LEO inhibited P. gingivalis hemagglutination, hemolysis (p < 0.05), and heme accumulation. Moreover, biofilm formation was significantly reduced by over 85% at 1/2 MIC though suppression of autoaggregation and hydrophobicity (p < 0.05). Molecular docking analysis predicted that α-citral (46.41%) and neral (31.58%), the major metabolites of LEO, may act as potential bioactive metabolites. In addition, LEO significantly reduced the levels of pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6), notably decreasing TNF-α secretion to 0.82× and 0.66× (MIC and MBC, respectively) relative to the LPS group (p < 0.05). It also alleviated oxidative stress through slc7a11 upregulation and subsequent glutathione synthesis, leading to restoration of the GSH/GSSG ratio and a reduction in ROS and MDA levels (p < 0.05). Moreover, LEO downregulated Tfrc expression and decreased Fe²⁺ accumulation (p < 0.05), suggesting its potential role in restoring iron homeostasis and suppressing ferroptosis-associated markers, such as Ptgs2. These effects highlight the multifunctional regulatory capacity of LEO during P. gingivalis-LPS-induced inflammatory stress.

Conclusion

LEO demonstrated multitarget inhibitory effects by attenuating P. gingivalis virulence and regulating macrophage oxidative and iron homeostasis. These findings support its potential as a natural adjunctive or preventive agent in periodontitis therapy.