Cinnamomum verum extract inhibits NOX2/ROS and PKCδ/JNK/AP-1/NF-κB pathway-mediated inflammatory response in PMA-stimulated THP-1 monocytes

Cinnamomum verum J. Presl (Cinnamon) is widely used in the food and pharmaceutical industries. C. verum exhibits various biological activities. However, it is unclear whether C. verum can inhibit NOX, a major source of ROS generation, and exert anti-inflammatory and antioxidant effects in PMA-stimul...

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Veröffentlicht in:Phytomedicine (Stuttgart) 2023-04, Vol.112, p.154685-154685, Article 154685
Hauptverfasser: Kim, Na-Yeon, Kim, Seonhwa, Park, Hyo-Min, Lim, Chae-Min, Kim, Jinju, Park, Jae-Young, Jeon, Kyeong-Bae, Poudel, Amrit, Lee, Hee Pom, Oh, Sei-Ryang, Ahn, Jongmin, Yoon, Do-Young
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Sprache:eng
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Zusammenfassung:Cinnamomum verum J. Presl (Cinnamon) is widely used in the food and pharmaceutical industries. C. verum exhibits various biological activities. However, it is unclear whether C. verum can inhibit NOX, a major source of ROS generation, and exert anti-inflammatory and antioxidant effects in PMA-stimulated THP-1 cells. This study investigates the anti-inflammatory and antioxidant effects of C. verum in PMA-stimulated THP-1 cells. The MeOH extract of C. verum was analyzed using UPLC-QTOF/MS. Anti-inflammatory and antioxidant effects of C. verum extract were examined by DCF-DA staining, immunofluorescence staining, RT-PCR, and immunoblotting in PMA-stimulated THP-1 cells. C. verum and its components, cinnamic acid and coumarin, significantly attenuated the expression of IL-1β, IL-8, CCL5, and COX-2 in PMA-stimulated THP-1. C. verum decreased ROS levels via NOX2 downregulation, as well as ameliorated plasma membrane translocation of PKCδ and decreased JNK phosphorylation. Besides, C. verum suppressed the nuclear translocation of AP-1 and NF-κB, which modulates diverse pro-inflammatory genes. C. verum effectively inhibits inflammation and oxidative stress during monocyte-macrophage differentiation and downregulates inflammatory mediators via NOX2/ROS and PKCδ/JNK/AP-1/NF-κB signaling. [Display omitted]
ISSN:0944-7113
1618-095X
DOI:10.1016/j.phymed.2023.154685