Allergic asthma is characterized by hyperresponsiveness and inflammation of the airway with increased expression of inducible nitric oxide synthase (iNOS) and overproduction of nitric oxide (NO). Grape seed proanthocyanidin extract (GSPE) has been proved to have antioxidant, antitumor, anti-inflammatory, and other pharmacological effects. The purpose of this study was to examine the role of GSPE on airway inflammation and hyperresponsiveness in a mouse model of allergic asthma. BALB/c mice, sensitized and challenged with ovalbumin (OVA), were intraperitoneally injected with GSPE. Administration of GSPE remarkably suppressed airway resistance and reduced the total inflammatory cell and eosinophil counts in BALF. Treatment with GSPE significantly enhanced the interferon (IFN)- γ level and decreased interleukin (IL)-4 and IL-13 levels in BALF and total IgE levels in serum. GSPE also attenuated allergen-induced lung eosinophilic inflammation and mucus-producing goblet cells in the airway. The elevated iNOS expression observed in the OVA mice was significantly inhibited by GSPE. In conclusion, GSPE decreases the progression of airway inflammation and hyperresponsiveness by downregulating the iNOS expression, promising to have a potential in the treatment of allergic asthma.
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http://dx.doi.org/10.1055/s-0030-1270957 | DOI Listing |
Inflamm Res
January 2025
Guangdong Provincial Key Laboratory of Medical Immunology and Molecular Diagnostics, The First Dongguan Affiliated Hospital, College of Medical Technology, Guangdong Medical University, Dongguan, 523808, China.
Allergic asthma is a chronic complex airway disease characterized by airway hyperresponsiveness, eosinophilic inflammation, excessive mucus secretion, and airway remodeling, with increasing mortality and incidence globally. The pathogenesis of allergic asthma is influenced by various factors including genetics, environment, and immune responses, making it complex and diverse. Recent studies have found that various cellular functions of mitochondria such as calcium regulation, adenosine triphosphate production, changes in redox potential, and free radical scavenging, are involved in regulating the pathogenesis of asthma.
View Article and Find Full Text PDFAm J Respir Cell Mol Biol
January 2025
Lady Davis Institute for Medical Research, Montreal, Quebec, Canada;
Iron regulatory protein 2 (IRP2), a post-transcriptional regulator of cellular iron metabolism has been associated with susceptibility to chronic obstructive pulmonary disease (COPD). Resistive breathing (RB) is the hallmark of the pathophysiology of obstructive airway diseases, especially during exacerbations, where increased mechanical stress is imposed on the lung. We have previously shown that RB, through tracheal banding, mimicking severe airway obstruction, induces pulmonary inflammation and injury in previously healthy mice.
View Article and Find Full Text PDFIntroduction And Objectives: The fractional exhaled fraction of nitric oxide (FeNO) is used in clinical practice for asthma diagnosis, phenotyping, and therapeutic management. Therefore, accurate thresholds are crucial. The normal FeNO values over lifespan in a respiratory healthy population and the factors related to them remain unclear.
View Article and Find Full Text PDFPediatr Pulmonol
January 2025
The Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
Background: Respiratory syncytial virus (RSV) infection in the first year of life has been linked with an increased risk for asthma. Some propose that RSV-induced inflammation leads to lasting airway changes, while others contend that RSV bronchiolitis is a marker for underlying predisposition. Social distancing adopted during the COVID-19 pandemic has led to a dramatic reduction in RSV activity, providing an unexpected opportunity to investigate this debate.
View Article and Find Full Text PDFOpen Respir Arch
November 2024
Translational Research In Airway Diseases Group (TRIAD), Health Research Institute of Santiago de Compostela (IDIS), Santiago de Compostela, Spain.
Respiratory diseases and cardiovascular diseases (CVDs) have high prevalence and share common risk factors. In some respiratory diseases such as sleep apnoea and COPD, the evidence of their negative impact on the prognosis of CVDs seems clear. However, in other diseases it is less evident whether there is any direct relationship.
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