What is the clinical evidence from this study?

Study design: Other. Population: Tracheal stenosis. Intervention: Quercetin vs. Control / PI3K inhibitor. Primary outcome: Macrophage polarization and α-SMA expression.

What does this research mean for the field?

Quercetin improves tracheal stenosis following injury by regulating macrophage polarization through the modulation of the PI3K/Akt signaling pathway. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To investigate whether quercetin attenuates tracheal stenosis after injury by regulating macrophage polarization through the PI3K/Akt signaling pathway.

September 10, 2026Natural Product CommunicationsOpen Access

Quercetin Regulates Macrophage Polarization via the PI3K/Akt Signaling Pathway and Improves Stenosis After Tracheal Injury

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Key result

Quercetin improves tracheal stenosis by reducing α-SMA expression and regulating macrophage polarization via PI3K/Akt signaling.

Why the study?

The study was conducted to investigate how quercetin improves tracheal stenosis by modulating macrophage polarization via the PI3K/Akt signaling pathway.

Population

Rabbits with a tracheal stenosis model and RAW264.7 macrophages

Comparison

Quercetin and PI3K inhibitor treatments across experimental groups

Design

Animal and in vitro controlled experimental study

Authors

JGJinghua Gan GLGuangnan Liu

Discussion

Member takes

Overview

Hypothesis-generating for quercetin in tracheal stenosis; prospective human trials needed before any clinical consideration.

Key Points

To investigate whether quercetin attenuates tracheal stenosis after injury by regulating macrophage polarization through the PI3K/Akt signaling pathway.
Established a rabbit model of tracheal stenosis across five experimental groups and assessed α-SMA expression in mucosal tissue using immunofluorescence.
Cultured RAW264.7 macrophages with quercetin and a PI3K inhibitor to evaluate cell morphology, M1/M2 surface markers, cytokine expression, and PI3K/Akt signaling pathway activity.
Co-cultured M1 and M2 macrophages with fibroblasts in equal proportions and quantified α-SMA mRNA levels via real-time PCR.
Quercetin treatment reduced α-SMA expression in rabbit tracheal mucosa and shifted macrophage morphology toward an M2 anti-inflammatory phenotype, achieving an M2/M1 ratio near 1.0.
Quercetin downregulated pro-inflammatory markers iNOS and TNF-α while upregulating anti-inflammatory markers Arg1 and IL-10, an effect modulated by PI3K inhibition.
In tracheal stenosis tissue, quercetin downregulated Akt1 and upregulated Akt2 and Akt3, while co-culturing balanced M1/M2 macrophages with fibroblasts suppressed fibrotic α-SMA mRNA expression.

PICO

Population

In vivo rabbit model of tracheal stenosis and in vitro RAW264.7 macrophages used to study the effects of quercetin.

Intervention / Comparator

Quercetin vs Control / PI3K inhibitor

Primary Outcome

Macrophage polarization and α-SMA expression

Cite This Study

Gan et al. (2026) studied Tracheal stenosis. Quercetin vs. Control / PI3K inhibitor was evaluated on Macrophage polarization and α-SMA expression. Quercetin improved tracheal stenosis by reducing α-SMA expression and regulating macrophage polarization (M2/M1 ratio approaching 1.0) via the PI3K/Akt signaling pathway.

synapsesocial.com/papers/6aa269eaa1e7502606509ffd https://doi.org/10.1177/1934578x261486102

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September 10, 2026Natural Product CommunicationsOpen Access

Quercetin Regulates Macrophage Polarization via the PI3K/Akt Signaling Pathway and Improves Stenosis After Tracheal Injury

View Full Paper

Ask AI

Bookmark

Key result

Quercetin improves tracheal stenosis by reducing α-SMA expression and regulating macrophage polarization via PI3K/Akt signaling.

Why the study?

The study was conducted to investigate how quercetin improves tracheal stenosis by modulating macrophage polarization via the PI3K/Akt signaling pathway.

Population

Rabbits with a tracheal stenosis model and RAW264.7 macrophages

Comparison

Quercetin and PI3K inhibitor treatments across experimental groups

Design

Animal and in vitro controlled experimental study

Authors

JGJinghua Gan GLGuangnan Liu

Discussion

Member takes

Overview

Hypothesis-generating for quercetin in tracheal stenosis; prospective human trials needed before any clinical consideration.

Key Points

To investigate whether quercetin attenuates tracheal stenosis after injury by regulating macrophage polarization through the PI3K/Akt signaling pathway.
Established a rabbit model of tracheal stenosis across five experimental groups and assessed α-SMA expression in mucosal tissue using immunofluorescence.
Cultured RAW264.7 macrophages with quercetin and a PI3K inhibitor to evaluate cell morphology, M1/M2 surface markers, cytokine expression, and PI3K/Akt signaling pathway activity.
Co-cultured M1 and M2 macrophages with fibroblasts in equal proportions and quantified α-SMA mRNA levels via real-time PCR.
Quercetin treatment reduced α-SMA expression in rabbit tracheal mucosa and shifted macrophage morphology toward an M2 anti-inflammatory phenotype, achieving an M2/M1 ratio near 1.0.
Quercetin downregulated pro-inflammatory markers iNOS and TNF-α while upregulating anti-inflammatory markers Arg1 and IL-10, an effect modulated by PI3K inhibition.
In tracheal stenosis tissue, quercetin downregulated Akt1 and upregulated Akt2 and Akt3, while co-culturing balanced M1/M2 macrophages with fibroblasts suppressed fibrotic α-SMA mRNA expression.

PICO

Population

In vivo rabbit model of tracheal stenosis and in vitro RAW264.7 macrophages used to study the effects of quercetin.

Intervention / Comparator

Quercetin vs Control / PI3K inhibitor

Primary Outcome

Macrophage polarization and α-SMA expression

Cite This Study

synapsesocial.com/papers/6aa269eaa1e7502606509ffd https://doi.org/10.1177/1934578x261486102

Also Consider

Synapse has enriched 2 closely related papers on similar clinical questions. Consider them for comparative context:

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