ArticleGenes and immunity2025
Abnormal activation of platelets and inflammation in smoking-induced rheumatoid arthritis is alleviated by 3,3'-diindolylmethane.
Article in Genes and immunity, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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
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