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Sulforaphene Mitigates Periodontitis by NRF2‐Dependent Regulation of P. gingivalis‐Induced Inflammatory Response and Bone Homeostasis.

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Title: Sulforaphene Mitigates Periodontitis by NRF2‐Dependent Regulation of P. gingivalis‐Induced Inflammatory Response and Bone Homeostasis.
Authors: Yao, Hantao1,2 (AUTHOR), Yu, Kai1 (AUTHOR), Jiang, Bulin1,2 (AUTHOR), Liao, Yilin1 (AUTHOR), Zhao, Yaoyu1 (AUTHOR), Chen, Jingqiu1 (AUTHOR), Li, Ting1 (AUTHOR), Yin, Mengjie1 (AUTHOR), Sheng, Yue1 (AUTHOR), Ye, Wengwanyue1 (AUTHOR), Zhao, Boxuan1 (AUTHOR), Du, Minquan1 (AUTHOR) duminquan@whu.edu.cn, Ji, Yaoting1 (AUTHOR) yaotingji@whu.edu.cn
Source: Food Science & Nutrition. Dec2025, Vol. 13 Issue 12, p1-19. 19p.
Subject Terms: Periodontitis, Nuclear factor E2 related factor, Anti-inflammatory agents, Inflammation, Bone metabolism, Gingiva, Cytokines, Therapeutics
Abstract: Periodontitis is a prevalent chronic inflammatory disease closely associated with various systemic disorders. Conventional therapies, including mechanical debridement and antibiotics, are often insufficient to fully resolve inflammation or restore bone homeostasis. Sulforaphene (LFS) is abundant in radish seed oil and Lai Fu‐zi, a traditional Chinese herbal medicine and has been recognized for its anti‐inflammatory potential. Here, we show that LFS markedly attenuates the secretion of pro‐inflammatory cytokines (IL‐1β, IL‐6, and IL‐8) from human gingival fibroblasts and inhibits osteoclast differentiation even under IL‐1β‐induced inflammatory conditions, without compromising the osteogenic capacity of periodontal ligament cells (PDLC). Mechanistically, LFS activates the NRF2 pathway and its protective effect against alveolar bone loss was evident in Nrf2+/+ mice but not Nrf2−/− mice. Notably, LFS was also found to inhibit the growth, virulence, and biofilm formation of P. gingivalis in vitro, and reduced its abundance within the subgingival microbiota in vivo. Together, these findings identify LFS as a potent NRF2‐dependent modulator, offering a promising therapeutic strategy for the prevention and treatment of periodontitis. [ABSTRACT FROM AUTHOR]
Copyright of Food Science & Nutrition is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: Sulforaphene Mitigates Periodontitis by NRF2‐Dependent Regulation of P. gingivalis‐Induced Inflammatory Response and Bone Homeostasis.
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  Data: <searchLink fieldCode="JN" term="%22Food+Science+%26+Nutrition%22">Food Science & Nutrition</searchLink>. Dec2025, Vol. 13 Issue 12, p1-19. 19p.
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  Data: <searchLink fieldCode="DE" term="%22Periodontitis%22">Periodontitis</searchLink><br /><searchLink fieldCode="DE" term="%22Nuclear+factor+E2+related+factor%22">Nuclear factor E2 related factor</searchLink><br /><searchLink fieldCode="DE" term="%22Anti-inflammatory+agents%22">Anti-inflammatory agents</searchLink><br /><searchLink fieldCode="DE" term="%22Inflammation%22">Inflammation</searchLink><br /><searchLink fieldCode="DE" term="%22Bone+metabolism%22">Bone metabolism</searchLink><br /><searchLink fieldCode="DE" term="%22Gingiva%22">Gingiva</searchLink><br /><searchLink fieldCode="DE" term="%22Cytokines%22">Cytokines</searchLink><br /><searchLink fieldCode="DE" term="%22Therapeutics%22">Therapeutics</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Periodontitis is a prevalent chronic inflammatory disease closely associated with various systemic disorders. Conventional therapies, including mechanical debridement and antibiotics, are often insufficient to fully resolve inflammation or restore bone homeostasis. Sulforaphene (LFS) is abundant in radish seed oil and Lai Fu‐zi, a traditional Chinese herbal medicine and has been recognized for its anti‐inflammatory potential. Here, we show that LFS markedly attenuates the secretion of pro‐inflammatory cytokines (IL‐1β, IL‐6, and IL‐8) from human gingival fibroblasts and inhibits osteoclast differentiation even under IL‐1β‐induced inflammatory conditions, without compromising the osteogenic capacity of periodontal ligament cells (PDLC). Mechanistically, LFS activates the NRF2 pathway and its protective effect against alveolar bone loss was evident in Nrf2+/+ mice but not Nrf2−/− mice. Notably, LFS was also found to inhibit the growth, virulence, and biofilm formation of P. gingivalis in vitro, and reduced its abundance within the subgingival microbiota in vivo. Together, these findings identify LFS as a potent NRF2‐dependent modulator, offering a promising therapeutic strategy for the prevention and treatment of periodontitis. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Food Science & Nutrition is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1002/fsn3.71319
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      – Code: eng
        Text: English
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        PageCount: 19
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      – SubjectFull: Periodontitis
        Type: general
      – SubjectFull: Nuclear factor E2 related factor
        Type: general
      – SubjectFull: Anti-inflammatory agents
        Type: general
      – SubjectFull: Inflammation
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      – SubjectFull: Bone metabolism
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      – SubjectFull: Gingiva
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              M: 12
              Text: Dec2025
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