# Suppression of LPS-Induced Inflammation by Phragmites communis Young Leaf Extract via Multi-Target Inhibition of IκB, AP-1, and STAT1/3 Pathways in RAW 264.7 Cells

## TL;DR

This study shows that young reed leaves reduce inflammation by blocking key inflammatory pathways in immune cells.

## Contribution

The study reveals the anti-inflammatory mechanisms of Phragmites communis young leaf extract through multi-target pathway inhibition.

## Key findings

- PCE reduced NO and pro-inflammatory cytokines by 40–60% in LPS-stimulated macrophages.
- PCE inhibited IκBα, AP-1, and STAT1/3 pathways while upregulating HO-1 expression.
- The extract showed no cytotoxicity up to 100 μg/mL and suppressed inflammatory mediator production.

## Abstract

Young leaves of reed (Phragmites communis) have been reported to exhibit antioxidant effects; however, their anti-inflammatory properties have not yet been investigated. In this study, we evaluated the effects of young reed leaf extract (PCE) on LPS-induced inflammation in RAW 264.7 cells and elucidated the underlying molecular mechanisms. Our results demonstrate that PCE significantly inhibited the production of nitric oxide (NO) by approximately 45% at 100 μg/mL (p < 0.01) and pro-inflammatory cytokines such as IL-6, TNF-α, and GM-CSF by 40–60% (p < 0.01) in LPS-stimulated RAW 264.7 macrophages, without cytotoxicity up to 100 μg/mL. PCE also downregulated the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and upregulated heme oxygenase-1 (HO-1) expression by approximately 2-fold at 100 μg/mL (p < 0.05). Mechanistically, these effects were associated with the inhibition of IκBα phosphorylation/degradation, IKKα/β phosphorylation, and AP-1 activation via the suppression of JNK and ERK signaling pathways, as well as the inhibition of STAT1/3 phosphorylation. Collectively, our findings suggest that PCE exerts anti-inflammatory effects by modulating the IκB, AP-1, and STAT1/3 signaling pathways, thereby suppressing inflammatory mediator production and enhancing antioxidant defense mechanisms in LPS-treated macrophages.