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<p>Rheumatoid arthritis (RA) is generally recognized as a complex disease initiated by environmental factors in the context of genetic susceptibility, among which smoking is one of the independent risk factors for RA. Smoking exposure would promote RA inflammation amplification probably because of platelet abnormal activation. This study aims to discover the preventive bioactivities of 3,3′-diindolylmethane (DIM) against RA with smoke exposure and explore the mechanisms by targeting platelet. The findings demonstrate that DIM can ameliorate smoking induced inflammation amplification in CIA mice through diverse of pathology analysis. Notably, the platelet abnormal activation was observed in CIA mice with smoke exposure and it was indeed inhibited by DIM treatment. Additionally, in vitro cigarette smoke extract (CSE) promoted platelet abnormal activation and aggregation characterizing by up-regulation of CD62p expression, Ca<sup>2+</sup> mobilization, ROS release and down-regulation of mitochondrial membrane potential (ΔΨm), while DIM could suppress these processes. We verified DIM could mitigate RA inflammation amplification induced by smoking and smoke exposure via inhibiting MAPK/NF-κB and PI3K/Akt/mTOR pathways phosphorylation during platelets abnormal activation. Our research provided a scientific basis for the rational use of DIM and other phytochemicals in the prevention and treatment of RA with smoking and smoke exposure from the perspective of nutrition.</p><p></p>

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Abnormal activation of platelets and inflammation in smoking-induced rheumatoid arthritis is alleviated by 3,3′-diindolylmethane

  • 期刊论文

  • 发表日期：

    2025年10月11日

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  • Bo Cai,
  • Yizheng You,
  • Longbo Huang,
  • Cheng Zhu,
  • Haofeng Lin,
  • Jinyang Chen,
  • Ruitao Ye,
  • Zhou Zhou,
  • Yibin Huang,
  • Longying Zha,
  • Ligang Jie,
  • Du Hongyan

摘要

Rheumatoid arthritis (RA) is generally recognized as a complex disease initiated by environmental factors in the context of genetic susceptibility, among which smoking is one of the independent risk factors for RA. Smoking exposure would promote RA inflammation amplification probably because of platelet abnormal activation. This study aims to discover the preventive bioactivities of 3,3′-diindolylmethane (DIM) against RA with smoke exposure and explore the mechanisms by targeting platelet. The findings demonstrate that DIM can ameliorate smoking induced inflammation amplification in CIA mice through diverse of pathology analysis. Notably, the platelet abnormal activation was observed in CIA mice with smoke exposure and it was indeed inhibited by DIM treatment. Additionally, in vitro cigarette smoke extract (CSE) promoted platelet abnormal activation and aggregation characterizing by up-regulation of CD62p expression, Ca2+ mobilization, ROS release and down-regulation of mitochondrial membrane potential (ΔΨm), while DIM could suppress these processes. We verified DIM could mitigate RA inflammation amplification induced by smoking and smoke exposure via inhibiting MAPK/NF-κB and PI3K/Akt/mTOR pathways phosphorylation during platelets abnormal activation. Our research provided a scientific basis for the rational use of DIM and other phytochemicals in the prevention and treatment of RA with smoking and smoke exposure from the perspective of nutrition.