Bark Extracts of <i>Chamaecyparis obtusa</i> (Siebold & Zucc.) Endl. Attenuate LPS-Induced Inflammatory Responses in RAW264.7 Macrophages

<i>Chamaecyparis obtusa</i> (Siebold & Zucc.) Endl. (<i>C. obtusa</i>) is an evergreen conifer native to temperate regions such as South Korea and Japan, traditionally used for its anti-inflammatory properties. However, the molecular mechanisms underlying the anti-inflamm...

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Main Authors: Bo-Ae Kim, Ji-A Byeon, Young-Ah Jang, Yong-Jin Kwon
Format: Article
Language:English
Published: MDPI AG 2025-07-01
Series:Plants
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Online Access:https://www.mdpi.com/2223-7747/14/15/2346
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Summary:<i>Chamaecyparis obtusa</i> (Siebold & Zucc.) Endl. (<i>C. obtusa</i>) is an evergreen conifer native to temperate regions such as South Korea and Japan, traditionally used for its anti-inflammatory properties. However, the molecular mechanisms underlying the anti-inflammatory effects of <i>C. obtusa</i> bark extracts remain poorly understood. In this study, I compared the biological activities of <i>C. obtusa</i> bark extracts prepared using boiling water (COWB) and 70% ethanol (COEB), and investigated their anti-inflammatory mechanisms in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. COEB significantly suppressed both mRNA and protein expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), along with decreased production of their respective inflammatory mediators, nitric oxide (NO) and prostaglandin E<sub>2</sub> (PGE<sub>2</sub>). Additionally, COEB selectively downregulated interleukin (IL)-1β expression, without affecting tumor necrosis factor-α (TNF-α), and unexpectedly upregulated IL-6. Notably, COEB did not inhibit the LPS-induced activation of major inflammatory signaling pathways, including mitogen-activated protein kinase (MAPK), nuclear factor-kappa B (NF-κB), and Janus kinase/signal transducer and activator of transcription (JAK/STAT). These findings suggest that COEB exerts anti-inflammatory effects by modulating key inflammatory mediators independently of canonical signaling pathways and may offer a novel therapeutic strategy for controlling inflammation.
ISSN:2223-7747