# Investigating the Therapeutic Potential of Agarwood Nanoemulsion in Modulating TGF-β-Induced Airway Remodelling in BEAS-2B Cells

## TL;DR

This study explores how Agarwood Nanoemulsion may help reduce airway changes caused by TGF-β in lung cells, offering a new approach to treating chronic respiratory diseases.

## Contribution

The study introduces Agarwood Nanoemulsion as a novel therapeutic candidate targeting TGF-β-induced airway remodelling.

## Key findings

- Agarwood Nanoemulsion reduces TGF-β-induced oxidative stress and restores nitric oxide production in BEAS-2B cells.
- AW-NE inhibits TGF-β-induced cell migration and decreases key inflammatory proteins like MMP-9, angiogenin, and PTX-3.
- The findings suggest AW-NE addresses underlying pathophysiology rather than just symptoms of respiratory diseases.

## Abstract

Chronic respiratory diseases such as asthma, chronic obstructive pulmonary disease (COPD), and pulmonary fibrosis are significant global health concerns, characterised by inflammation, oxidative stress, and airway remodelling. These processes are driven by multiple cytokines, with transforming growth factor-beta (TGF-β) playing a central role in the remodelling process. TGF-β triggers pathways that promote epithelial-mesenchymal transition (EMT), excessive extracellular matrix deposition, and increased oxidative stress, all of which contribute to airway remodelling. Despite availability of therapies including corticosteroids and bronchodilators that offer symptomatic relief, these fail to address the underlying causes of oxidative damage, persistent inflammation, and fibrosis, limiting long-term effectiveness. This study investigates the effects of Agarwood Nanoemulsion (AW-NE) on TGF-β-induced oxidative stress, inflammation, and airway remodelling in BEAS-2B cells, in vitro. The results show that AW-NE significantly reduces oxidative stress and restores nitric oxide (NO) production, suppressed by TGF-β activation. AW-NE also inhibits TGF-β-induced cell migration, indicating potential in modulating TGF-β-induced airway remodelling. Additionally, AW-NE treatment decreased the expression of key inflammatory and pro-remodelling proteins, including MMP-9, angiogenin, and pentraxin-3 (PTX-3). These findings suggest that, while current treatments primarily manage symptoms, AW-NE shows potential in addressing the underlying pathophysiology. Further in vivo studies are required to confirm its therapeutic efficacy.