Fisetin reduces ovalbumin-triggered airway remodeling by preventing phenotypic switching of airway smooth muscle cells.

ABSTRACT:

Background

The transformation of airway smooth muscle cells (ASMCs) from a quiescent phenotype to a hypersecretory and hypercontractile phenotype is a defining feature of asthmatic airway remodeling. Fisetin, a flavonoid compound, possesses anti-inflammatory characteristics in asthma; yet, its impact on airway remodeling and ASMCs phenotype transition has not been investigated.

Objectives

This research seeked to assess the impact of fisetin on ovalbumin (OVA) induced asthmatic airway remodeling and ASMCs phenotype transition, and clarify the mechanisms through network pharmacology predictions as well as in vivo and in vitro validation.

Methods

First, a fisetin-asthma-ASMCs network was constructed to identify potential targets. Subsequently, cellular and animal studies

SUBMITTER: Liu Y 

PROVIDER: S-EPMC11479573 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature