This study aimed to evaluate the effect of sanguinarine on biomechanical properties of rat airway smooth muscle cells (rASMCs) including stiffness, traction force and cytoskeletal stress fiber organization. To do so, rASMCs cultured were treated with sanguinarine solution at different concentrations (0.005~5 μmol/L) for 12 h, 24 h, 36 h, and 48 h, respectively. Subsequently, the cells were tested for their viability, stiffness, traction force, migration and microfilament distribution by using methylthiazolyldiphenyl-tetrazolium bromide assay, optical magnetic twisting cytometry, Fourier transform traction microscopy, scratch wound healing method, and immunofluorescence microscopy, respectively. The results showed that at concentration below 0.5 μmol/L sanguinarine had no effect on cell viability, but caused dose and time dependent effect on cell biomechanics. Specifically, rASMCs treated with sanguinarine at 0.05 μmol/L and 0.5 μmol/L for 12 and 24 h exhibited significant reduction in stiffness, traction force and migration speed, together with disorganization of the cytoskeletal stress fibers. Considering the essential role of airway smooth muscle cells (ASMCs) biomechanics in the airway hyperresponsiveness (AHR) of asthma, these findings suggest that sanguinarine may ameliorate AHR via alteration of ASMCs biomechanical properties, thus providing a novel approach for asthma drug development.
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http://dx.doi.org/10.7507/1001-5515.201708025 | DOI Listing |
Exp Physiol
January 2025
Robinson Research Institute, University of Adelaide, Adelaide, South Australia, Australia.
The mechanisms linking maternal asthma (MA) exposure in utero and subsequent risk of asthma in childhood are not fully understood. Pathological airway remodelling, including reticular basement membrane thickening, has been reported in infants and children who go on to develop asthma later in childhood. This suggests altered airway development before birth as a mechanism underlying increased risk of asthma in children exposed in utero to MA.
View Article and Find Full Text PDFRationale: Airflow obstruction refractory to β2 adrenergic receptor (β2AR) agonists is an important clinical feature of infant respiratory syncytial virus (RSV) bronchiolitis, with limited treatment options. This resistance is often linked to poor drug delivery and potential viral infection of airway smooth muscle cells (ASMCs). Whether RSV inflammation causes β2AR desensitization in infant ASMCs is unknown.
View Article and Find Full Text PDFInt J Biol Macromol
January 2025
School of Health Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan, Malaysia. Electronic address:
Asthma is a chronic respiratory disease characterized by airway inflammation. Lignosus rhinocerotis (LR), a medicinal mushroom rich in polysaccharide, has been traditionally used to treat various diseases, including asthma. This study aimed to fractionate, characterize and evaluate the anti-asthmatic effects of polysaccharides from LR (LRP).
View Article and Find Full Text PDFJ Asthma Allergy
January 2025
Amgen Inc., Thousand Oaks, CA, USA.
Airway inflammation, a hallmark feature of asthma, drives many canonical features of the disease, including airflow limitation, mucus plugging, airway remodeling, and hyperresponsiveness. The T2 inflammatory paradigm is firmly established as the dominant mechanism of asthma pathogenesis, largely due to the success of inhaled corticosteroids and biologic therapies targeting components of the T2 pathway, including IL-4, IL-5, IL-13, and thymic stromal lymphopoietin (TSLP). However, up to 30% of patients may lack signatures of meaningful T2 inflammation (ie, T2 low).
View Article and Find Full Text PDFImmunol Invest
January 2025
Department of Respiratory Medicine, First Affiliated Hospital, Heilongjiang University of Chinese Medicine, Harbin, China.
Introduction: T helper 17 (Th17) cells have a significant effect in the pathogenesis of asthma, and signal transducer and activator of transcription 3 (STAT3) pathway activation is critical for Th17 cell differentiation. Timosaponin A-III (TA3) was reported to inhibit the STAT3 pathway. Here, we investigated whether TA3 improved asthma by inhibiting the STAT3 pathway.
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