Anti-inflammatory effects of TP1 in LPS-induced Raw264.7 macrophages

Abstract Inflammation is an essential defense mechanism in health; however, excessive inflammation contributes to the pathophysiology of several chronic diseases. Although anti-inflammatory drugs are essential for controlling inflammation, they have several side effects. Recent findings suggest that...

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Bibliographic Details
Published in:Applied Biological Chemistry
Main Authors: Minji Kim, Jangeun An, Seong-Ah Shin, Sun Young Moon, Moonsu Kim, Seyeon Choi, Huiji Kim, Kim-Hoa Phi, Jun Hyuck Lee, Ui Joung Youn, Hyun Ho Park, Chang Sup Lee
Format: Article in Journal/Newspaper
Language:English
Published: SpringerOpen 2024
Subjects:
TP1
Anti-inflammation
NF-κB
MAPK
Agriculture (General)
S1-972
Chemistry
QD1-999
Antarc*
Antarctic
Online Access:https://doi.org/10.1186/s13765-024-00873-y
https://doaj.org/article/d03bc242df134b0aa21a2f4d2768f959
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Summary:Abstract Inflammation is an essential defense mechanism in health; however, excessive inflammation contributes to the pathophysiology of several chronic diseases. Although anti-inflammatory drugs are essential for controlling inflammation, they have several side effects. Recent findings suggest that naturally derived compounds possess physiological activities, including anti-inflammatory, antifungal, antiviral, anticancer, and immunomodulatory activities. Therefore, this study aimed to investigate the anti-inflammatory effects and molecular mechanisms of 2,5,6-trimethoxy-p-terphenyl (TP1), extracted from the Antarctic lichen Stereocaulon alpinum, using in vitro models. TP1 treatment decreased the production of nitric oxide (NO) and reactive oxygen species (ROS) in LPS-stimulated Raw264.7 macrophages. Additionally, TP1 treatment significantly decreased the mRNA levels of pro-inflammatory cytokines (IL-1β, TNF-α, IL-6) and the mRNA and protein levels of the pro-inflammatory enzymes (inducible nitric oxide synthase and cyclooxygenase-2). Moreover, TP1 suppressed lipopolysaccharide-induced phosphorylation of the NF-κB and MAPK signaling pathways in Raw264.7 macrophages. Conclusively, these results suggest that TP1 ameliorates inflammation by suppressing the expression of pro-inflammatory cytokines, making it a potential anti-inflammatory drug for the treatment of severe inflammatory diseases.

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