Background:Asthma is a common chronic respiratory disorder characterized by inflammation
and remodeling of the airways.Aims:This study aimed to identify the inhibitory effects of Huatan Tongluo decoction (HTTLD) on airway
inflammation and associated remodeling mechanisms.Methods:Mice were immunized with ovalbumin (OVA) for 8 weeks to generate chronic asthma mouse
models (CAS), which were randomly divided into 4 groups administrated with pachyman, dexamethasone
(DEX), HTTLD, and without anything (CAS model), while mice who administrated saline were assigned
as the control group. Hematoxylin-eosin (H&E) and Masson trichrome were used to determine inflammatory
infiltration and airway remodeling (fiber deposition). Inflammatory cytokines, including VEGF,
PDGF, and TGF-β1, were analyzed using ELISA. The gene transcriptions and expressions of MMP-9,
TIMP-1, VEGF, HIF-1α, NF-kB, and β-actin were evaluated using RT-PCR and Western blot, while the
expression of p-Smad2/3 was determined by Western blot.Results:HTTLD inhibited inflammatory infiltration and airway remodeling (reducing airway wall thickness
and decreasing fiber deposition) of lung tissues in the CAS mouse model. HTTLD markedly attenuated
levels of TGF-β1, VEGF, and PDGF compared to those of mice in the CAS model group (p < 0.05).
HTTLD significantly reduced the secretion of matrix metalloproteinases (MMP-9 and TIMP-1) and the
expression of NF-kB/HIF-1α compared to mice in the CAS model group (p < 0.05). HTTLD prominently
downregulated phosphorylated levels of the Smad2/3 molecule (ratio of p-Smad3/2/Smad2/3) compared
to mice in the CAS group (p < 0.05).Conclusion:HTTLD inhibited inflammatory infiltration and airway remodeling in an OVA-induced
chronic asthma mouse model by attenuating the TGF-β1/Smad2/3 signaling pathway and suppressing the
oxidative stress-mediated NF-kB/HIF-1α/MMPs signaling pathway.