Naturally derived bioactive compounds as regulators of oxidative stress and inflammation in asthma

Abstract

Asthma is a chronic allergic respiratory disease characterized by symptoms such as coughing, dyspnea, and reversible airway obstruction. The incidence of asthma has been gradually increasing worldwide. However, the pathophysiological mechanisms underlying its development remain unclear due to its multifactorial etiology, which encompasses genetic, environmental, and occupational factors. Furthermore, the clinical manifestations of asthma vary significantly among individuals and across age groups, often coexisting with symptoms of atopic dermatitis and allergic rhinitis, thereby necessitating a personalized and continuous therapeutic approach. Asthma management primarily involves the use of symptom relievers and anti-inflammatory controllers, including β₂-agonists, anticholinergics, and corticosteroids. However, prolonged or high-dose administration of these agents poses a risk of adverse effects. Given these limitations, the development of novel asthma therapies with enhanced efficacy and fewer side effects requires a deeper understanding of the pathophysiological mechanisms underlying the development of the disease. Existing evidence from various preclinical studies suggests that oxidative stress and inflammatory responses play pivotal roles in the onset and exacerbation of asthma. Therefore, the purpose of this review was to address the multifaceted pathological mechanisms of asthma, highlight naturally derived bioactive compounds with potential antioxidative and anti-inflammatory properties that could be beneficial for asthma management. Additionally, propose an integrative therapeutic strategy that enhances patient adherence while minimizing adverse effects, ultimately contributing to improved long-term management and treatment of asthma.

Keywords: Allergic respiratory disease; Asthma; Inflammation; Oxidative stress; Reactive oxygen species.

Fig. 1

Pathogenesis of asthma. Asthma is caused and exacerbated by repeated exposure to various harmful substances, including environmental pollutants, bacteria, microbes, and allergens. In addition, asthma is characterized by hypersensitivity and dysregulated immune responses mediated by pro-inflammatory mediators and activated immune cells, such as dendritic cells, eosinophils, mast cells, neutrophils, macrophages, and lymphocytes. Asthma becomes chronic and worsens as it progresses, leading to airway hyperresponsiveness and airway remodeling. Immunoglobulin E, IgE; interleukin, IL; type 2 innate lymphoid cell, ILC2; T helper, Th; thymic stromal lymphopoietin, TSLP. Created with BioRender.com. Accessed on 17 March 2025

Fig. 2

Etiology of asthma. Asthma is a chronic allergic respiratory disease with a highly complex and multifactorial etiology. The pathogenesis of asthma is broadly classified into host factors and environmental factors. The host factors include family history, genetic and epigenetic modifications, obesity, sex, aging, comorbidities, inflammation, and oxidative stress. The environmental factors encompass air pollution, smoking, viral infections, various allergens, and psychological stress. A comprehensive understanding of the interactions between pathogenic mechanisms is essential for the prevention, management, and treatment of asthma. Created with BioRender.com. Accessed on 17 March 2025