# Lipopolysaccharide-Induced Inflammatory Response and Its Prominent Suppression by Paspalum thunbergii Extract

## TL;DR

This paper shows that an extract from Paspalum thunbergii reduces inflammation by inhibiting key inflammatory pathways in cells.

## Contribution

The study identifies the anti-inflammatory mechanisms of Paspalum thunbergii extract through multiple signaling pathways.

## Key findings

- The extract inhibits LPS-induced NO production in RAW 264.7 cells.
- It suppresses the expression of iNOS and COX-2 enzymes.
- The extract inhibits multiple signaling pathways including MAPK, NF-κB, JAK/STAT, and Wnt/β-catenin.

## Abstract

The extract of Paspalum thunbergii, a native perennial herb in Korea belonging to the rice family, was investigated for its anti-inflammatory activity and the underlying mechanisms driving its effects. Fifteen chemical components of the P. thunbergii extract, including rosmarinic acid and isoquercitrin, were identified using LC-MS. The extract showed antioxidative activity through DPPH and ABTS cation radical scavenging activity. The P. thunbergii extract significantly inhibited lipopolysaccharide (LPS)-induced nitric oxide (NO) production in macrophage RAW 264.7 cells. The extract inhibited the expression of lipopolysaccharide-induced iNOS and COX-2, which are inflammation-related enzymes. To explore the underlying anti-inflammatory mechanism, the expression levels of signal proteins related to MAPK, NF-κB, JAK/STAT, and Wnt/β-catenin signaling were measured. As a result, the P. thunbergii extract inhibited the expression of p-p38, and p-JNK increased by LPS in RAW 264.7 cells. Additionally, it decreased the expression of LPS-induced p-IKKβ and p-NF-κB p65 and prevented the migration of p-NF-κB into the nucleus caused by LPS. Notably, p-JAK1, p-STAT3, Wnt 3α, β-catenin, and p-GSK-3β protein expressions were also inhibited. Therefore, the prominent anti-inflammatory activity of the P. thunbergii extract may be via the MAPK, NF-κB, JAK/STAT, Wnt/β-catenin signal pathway.