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·2025
Caulerpa okamurae extract alleviates pulmonary fibrosis in vitro and in vivo by modulating Tgfβ/SMAD/MAPK signaling and NLRP3 inflammasome activation
Seok Hee Seo, Thi My Tien Truong, Hyejin Hyeon, Young‐Min Ham, Yong‐Hwan Jung, Hyun‐Jin Kim, Dong-Shin Kim, Inhae Kang
Journal of Functional Foods
초록

Pulmonary fibrosis (PF) characterized by fibroblast dysfunction and inflammation, in driven by transforming growth factor beta (Tgf β ) plays a crucial role. Caulerpa okamurae extract (COE), drived from a green seaweed widely consumed in East Asia, is known for its anti-obesity properties, but its effects on PF remain unexplored. This study investigated the potential of the COE in PF using Tgf β -stimulated MRC-5 lung fibroblasts and bleomycin (BLM)-induced PF in C57BL/6 mice. In vitro , COE significantly reduced fibrotic markers ( α-Sma , Mmp1 , Col1a1 , and Vimentin ) and suppressed inflammatory mediators ( Il-1β , Il-6 , and Cox2 ) by downregulating Tgfβ/SMAD2/3 and MAPK signaling. In vivo , COE attenuated fibrotic features in BLM-treated mice by modulating the Tgf β /SMAD/MAPK pathway. Interestingly, COE decreased plasma levels of IL-1 β , an indicative of suppressed NLRP3 inflammasome activation. This effect was further validated in lipopolysaccharide and nigericin-treated bone marrow-derived macrophages, where COE inhibited NLRP3 inflammasome activation. These finding highlight COE's action in mitigating fibrosis and inflammation by modulation of Tgf β /SMAD2/3 and MAPK signaling, along with the NLRP3 inflammasome pathway, underscoring its potential as a novel therapeutic for PF. • Caulerpa okamurae extract (COE) mitigates pulmonary fibrosis in vivo and in vitro . • COE inhibited fibrosis markers by modulating TGFβ/SMAD/MAPK pathways. • COE lowered NLRP3 inflammasome activation.

키워드
InflammasomeSMADIn vivoMAPK/ERK pathwayPulmonary fibrosisSignal transductionTransforming growth factorPharmacologyIn vitroCell biology
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2025

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