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Background <p>Heterotopic ossification (HO) pathogenesis involves ROS-driven stem cell differentiation. Carnosic acid (CA), a natural antioxidant, remains unexplored for HO.</p> Methods <p>In vitro, tendon-derived stem cells (TDSCs) were stimulated with IL-1β, and CA was used for intervention to assess its effects on differentiation and ROS production via real-time quantitative PCR (qPCR), western blotting (WB), and immunofluorescence. Additionally, a burn and Achilles tendon transection-induced mouse model of traumatic HO was established to evaluate the therapeutic potential of CA.</p> Results <p>In vitro, CA activated nuclear factor erythroid 2-related factor 2 (Nrf2) and inhibited nicotinamide adenine dinucleotide phosphate oxidase 1 (NOX1), leading to increased antioxidant enzyme activity and reduced intracellular ROS levels. CA also regulated the PTEN/AKT signaling pathway, suppressing osteogenic and chondrogenic differentiation of TDSCs. In vivo, micro-computed tomography (Micro-CT) and histological analyses demonstrated that CA activated Nrf2 and enhanced antioxidant enzyme expression, thereby inhibiting osteogenic and chondrogenic factor expression in Achilles tendon tissue and reducing HO formation.</p> Conclusions <p>CA is a novel HO therapeutic by dual targeting of oxidative stress and differentiation pathways.</p>

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Carnosic acid serves as a dual Nrf2 activator and PTEN/AKT suppressor to inhibit traumatic heterotopic ossification

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月29日

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  • Donglei Wei,
  • Dezhi Song,
  • Hui Wang,
  • Yuangang Su,
  • Jiamin Liang,
  • Jiake Xu,
  • Jinmin Zhao,
  • Qian Liu

摘要

Background

Heterotopic ossification (HO) pathogenesis involves ROS-driven stem cell differentiation. Carnosic acid (CA), a natural antioxidant, remains unexplored for HO.

Methods

In vitro, tendon-derived stem cells (TDSCs) were stimulated with IL-1β, and CA was used for intervention to assess its effects on differentiation and ROS production via real-time quantitative PCR (qPCR), western blotting (WB), and immunofluorescence. Additionally, a burn and Achilles tendon transection-induced mouse model of traumatic HO was established to evaluate the therapeutic potential of CA.

Results

In vitro, CA activated nuclear factor erythroid 2-related factor 2 (Nrf2) and inhibited nicotinamide adenine dinucleotide phosphate oxidase 1 (NOX1), leading to increased antioxidant enzyme activity and reduced intracellular ROS levels. CA also regulated the PTEN/AKT signaling pathway, suppressing osteogenic and chondrogenic differentiation of TDSCs. In vivo, micro-computed tomography (Micro-CT) and histological analyses demonstrated that CA activated Nrf2 and enhanced antioxidant enzyme expression, thereby inhibiting osteogenic and chondrogenic factor expression in Achilles tendon tissue and reducing HO formation.

Conclusions

CA is a novel HO therapeutic by dual targeting of oxidative stress and differentiation pathways.