Airway smooth muscle in contractility and remodeling of asthma: potential drug target mechanisms

Khalfaoui, Latifa; Pabelick, Christina M.

doi:10.1080/14728222.2023.2177533

Cited by 14 publications

(1 citation statement)

References 182 publications

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“…Prolonged recurrence of asthma can lead to varying degrees of airway remodeling in affected individuals (Varricchi et al, 2022). Airway remodeling can result in alterations to airway function and organ properties, which is a crucial pathological factor leading to irreversible airway obstruction and hyperresponsiveness (Hsieh et al, 2023;Khalfaoui and Pabelick, 2023). Additionally, airway remodeling can exacerbate airway inflammation or secondary infection in asthma patients, and in severe cases, it may lead to increased mortality among those with asthma (Joseph and Tatler, 2022).…”

Section: Introductionmentioning

confidence: 99%

Effect of curcumin nanoparticles on proliferation and migration of mouse airway smooth muscle cells and airway inflammatory infiltration

Ma,

Ye,

Sun

et al. 2024

Front. Pharmacol.

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Curcumin (CUR) possesses the capability to inhibit various inflammatory factors, exert anti-inflammatory effects, and alleviate asthma attacks; however, its hydrophobicity and instability significantly impede its clinical application. In this study, we synthesized CUR-loaded nanoparticles (CUR-NPs) and evaluated their impact on the proliferation, migration, and inflammatory infiltration of mouse airway smooth muscle cells (ASMCs), while investigating their underlying mechanisms. To achieve this objective, ASMCs were isolated from BALB/c mice and subjected to TGF-β1-induced cell proliferation and migration. Our findings demonstrate that CUR-NPs effectively regulate the release of CUR within cells with superior intracellular uptake compared to free CUR. The CCK-8 assay results indicate that the blank carrier does not exhibit any cytotoxic effects on cells, thus rendering the impact of the carrier itself negligible. The TGF-β1 group exhibited a significant increase in cell proliferation, whereas treatment with CUR-NPs significantly suppressed TGF-β1-induced cell proliferation. The findings from both the cell scratch assay and transwell assay demonstrated that TGF-β1 substantially enhanced cell migration, while CUR-NPs treatment effectively attenuated TGF-β1-induced cell migration. The Western blot analysis demonstrated a substantial increase in the expression levels of TGF-β1, p-STAT3, and CTGF in ASMCs following treatment with TGF-β1 when compared to the control group. Nevertheless, this effect was effectively counteracted upon administration of CUR-NPs. Furthermore, an asthma mouse model was successfully established and CUR-NPs were administered through tail vein injection. The serum levels of TGF-β1 and the expression levels of TGF-β1, p-STAT3, and CTGF proteins in the lung tissue of mice in the model group exhibited significant increases compared to those in the control group. However, CUR-NPs treatment effectively attenuated this change. Our research findings suggest that CUR-NPs possess inhibitory effects on ASMC proliferation, migration, and inflammatory infiltration by suppressing activation of the TGF-β1/p-STAT3/CTGF signaling pathway, thereby facilitating inhibition of airway remodeling.

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