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<p>Periodontitis is a prevalent oral inflammatory condition and a major cause of tooth loss. This study sought to assess the impact of silymarin on LPS-triggered inflammatory responses in RAW 264.7 murine macrophages. The Osteoclast precursor cell line RAW264.7 was treated with lipopolysaccharide (LPS) to induce inflammation and cellular injury, and then with silymarin. Cell viability, apoptosis, autophagy, reactive oxygen species (ROS) production, proinflammatory cytokine levels, osteoclast formation, and protein levels in apoptotic, autophagic, and AMPK/Sirt1-autophagy axis were assessed using flow cytometry, Western blot analysis and CCK8 assay. LPS induced apoptosis, increased ROS production, triggered an inflammatory response, and reduced the viability of RAW 264.7 cells. Western blot analysis showed an elevation in Bax and cleaved caspase-3 expressions, while Bcl-2 levels decreased following LPS stimulation. After silymarin treatment, LPS-induced oxidative stress was reduced, and cell viability was improved. Meanwhile, the expressions of Bax and caspase-3 were downregulated. The LPS-induced inflammatory response was also reduced, resulting in lower levels of TNF-α, IL-6, and IL-1β, as well as downregulation of theNF-κB/Rel pathway. Conversely, silymarin administration enhanced autophagic activity in LPS-stimulated RAW 264.7 macrophages, as evidenced by elevated autophagosome formation and modulated expression of Beclin-1 and p62. Furthermore, silymarin suppressed RANKL-induced osteoclast differentiation in these cells, accompanied by reduced expression of osteoclast-specific markers. Notably, silymarin-treated cells exhibited increased AMPKα phosphorylation and upregulated Sirt1 levels, suggesting the activation of these regulatory pathways. This study demonstrates that silymarin alleviates LPS-induced cellular damage, inflammation, and suppresses RANKL-induced osteoclast differentiation in RAW 264.7 macrophages. These protective effects are closely associated with enhanced autophagic activity and the activation of the AMPK/Sirt1-autophagy regulatory axis. This study provides preliminary in vitro evidence that silymarin may have preclinical exploratory value for periodontitis intervention.</p>

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Silymarin inhibits osteoclastogenesis and alleviates inflammatory injury in RAW264.7 cells via activating the AMPK/Sirt1-autophagy axis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月6日

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  • Juan He,
  • Jianyong Kang,
  • Jing Zeng,
  • Jianqin Tan,
  • Mianmian Duan,
  • Yanyan Song

摘要

Periodontitis is a prevalent oral inflammatory condition and a major cause of tooth loss. This study sought to assess the impact of silymarin on LPS-triggered inflammatory responses in RAW 264.7 murine macrophages. The Osteoclast precursor cell line RAW264.7 was treated with lipopolysaccharide (LPS) to induce inflammation and cellular injury, and then with silymarin. Cell viability, apoptosis, autophagy, reactive oxygen species (ROS) production, proinflammatory cytokine levels, osteoclast formation, and protein levels in apoptotic, autophagic, and AMPK/Sirt1-autophagy axis were assessed using flow cytometry, Western blot analysis and CCK8 assay. LPS induced apoptosis, increased ROS production, triggered an inflammatory response, and reduced the viability of RAW 264.7 cells. Western blot analysis showed an elevation in Bax and cleaved caspase-3 expressions, while Bcl-2 levels decreased following LPS stimulation. After silymarin treatment, LPS-induced oxidative stress was reduced, and cell viability was improved. Meanwhile, the expressions of Bax and caspase-3 were downregulated. The LPS-induced inflammatory response was also reduced, resulting in lower levels of TNF-α, IL-6, and IL-1β, as well as downregulation of theNF-κB/Rel pathway. Conversely, silymarin administration enhanced autophagic activity in LPS-stimulated RAW 264.7 macrophages, as evidenced by elevated autophagosome formation and modulated expression of Beclin-1 and p62. Furthermore, silymarin suppressed RANKL-induced osteoclast differentiation in these cells, accompanied by reduced expression of osteoclast-specific markers. Notably, silymarin-treated cells exhibited increased AMPKα phosphorylation and upregulated Sirt1 levels, suggesting the activation of these regulatory pathways. This study demonstrates that silymarin alleviates LPS-induced cellular damage, inflammation, and suppresses RANKL-induced osteoclast differentiation in RAW 264.7 macrophages. These protective effects are closely associated with enhanced autophagic activity and the activation of the AMPK/Sirt1-autophagy regulatory axis. This study provides preliminary in vitro evidence that silymarin may have preclinical exploratory value for periodontitis intervention.