Platycodon grandiflorum Extract Alleviates Inflammation During Asthma Development In Vivo and In Vitro

TL;DR

This study shows that Platycodon grandiflorum extract reduces inflammation in asthma by affecting the TLR4/NF-κB pathway in both animal and cell experiments.

Contribution

The novel finding is that PGE reduces asthma-related inflammation via the TLR4/NF-κB pathway in both in vivo and in vitro models.

Findings

PGE treatment improved lung pathology and reduced inflammatory cell infiltration in asthmatic rats.

PGE decreased levels of pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 in asthma models.

PGE inhibited TLR4 and p-P65 expression, suggesting modulation of the TLR4/NF-κB pathway.

Abstract

Asthma causes over 1000 deaths daily worldwide and is becoming one of the most prevalent and severe respiratory diseases. This study aimed to investigate the therapeutic effects of Platycodon grandiflorum extract (PGE) on asthma both in vivo and in vitro.

Thirty Sprague–Dawley (SD) rats were divided into named control (NC), asthma, and PGE high-, medium-, and low-dose groups. The PGE groups were intragastrically administered the drug for 14 days. After treatment, pathological changes were observed using histological staining. Flow cytometry was used to observe changes in inflammatory cells. The expression of the toll-like receptor 4/nuclear factor kappa B (TLR4/NF-κB) pathway proteins was detected using western blotting. Additionally, lipopolysaccharide (LPS)-stimulated rat tracheal epithelial (RTE) cells were used for validation in vitro.

Histological staining revealed smooth muscle hyperplasia and inflammatory cell infiltration in asthmatic mice. The pathological condition of the lung tissue of rats in all treatment groups improved, with the high-dose group showing the most significant improvement. PGE treatment reduced the number of inflammatory cells recruited in the lung of asthmatic rats, and reduced tumor necrosis factor alpha (TNF-α), interleukin (IL)-1β, and IL-6 levels. Western blotting showed that TLR4 and p-P65 levels decreased significantly after PGE administration (p  < 0.05). Additionally, PGE treatment decreased apoptosis in LPS-stimulated RTE cells and decreased TNF-α, IL-1β, and IL-6 levels.

PGE inhibited inflammatory responses in asthmatic rats, which was validated at the cellular level. This therapeutic mechanism may be achieved through the regulation of the TLR4/NF-κB pathway.

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