# Edible Herb Aster glehni Alleviates Inflammation and Oxidative Stress in Chondrocytes by Regulating p38 and NF-κB Signaling Pathways with Partial Involvement of Its Major Component, 3,5-Dicaffeoylqunic Acid

## TL;DR

This study shows that Aster glehni extract reduces inflammation and oxidative stress in cartilage cells, potentially offering a new treatment for osteoarthritis.

## Contribution

The novel finding is that Aster glehni extract, but not its main compound 3,5-DCQA, inhibits inflammation and oxidative stress in chondrocytes via p38 and NF-κB pathways.

## Key findings

- A. glehni extract inhibits IL-6, COX-2, and MMP expressions in chondrocytes via p38 and NF-κB pathways.
- Extract reduces oxidative stress and prevents cell apoptosis in chondrocytes exposed to hydrogen peroxide.
- 3,5-DCQA partially replicates these effects only under short-term IL-1β stimulation.

## Abstract

Osteoarthritis (OA) is primarily a degenerative disease triggered by joint inflammation and oxidative stress. While Aster glehni is an edible and traditionally medicinal herb, the beneficial effect of A. glehni on OA progression remains unknown. This study aimed to investigate the effect of A. glehni extract (AGE) and its primary biological compound—3,5-dicaffeoylquinic acid (3,5-DCQA)—on inflammation and oxidative stress in chondrocytes. AGE effectively inhibited the expression of interleukin (IL)-6, cyclooxygenase (COX)-2, matrix metalloproteinase (MMP)-1, and MMP-13 in chondrocytes stimulated by IL-1β for 24 h. In contrast, 3,5-DCQA did not inhibit IL-6, COX-2, and MMP expressions under the same conditions. However, when chondrocytes were stimulated by IL-1β for a short duration (6 h), 3,5-DCQA suppressed IL-6, COX-2, and MMP expressions. The inhibition of IL-6, COX-2, and MMP expressions by AGE was associated with the p38 kinase and nuclear factor-κB signaling pathways, but not ERK and JNK signaling pathways. Furthermore, AGE prevented cell apoptosis and reduced intracellular reactive oxygen species levels in chondrocytes induced by hydrogen peroxide (H2O2). AGE restored the decreased superoxide dismutase 1 and catalase mRNA expressions caused by H2O2. Collectively, AGE may protect against cartilage deterioration by inhibiting inflammation and oxidative stress, making it a promising therapeutic agent for alleviating OA.