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Published on: September 22, 2023
The ALOX5-Mitochondrial oxidative stress link in quercetin-mediated nasal epithelial barrier protection in allergic
Mengfei Luo1, Xinyu Liu1, Fusen Peng1
1Department of Otolaryngology-Head and Neck Surgery, Loudi Central Hospital, Loudi, Hunan, 417000, PR China.
Objectives:
Allergic rhinitis (AR) is characterized by persistent allergic inflammation and nasal epithelial barrier dysfunction. Quercetin is a candidate bioactive compound of Hedyotis Diffusae Herba, but its epithelial mechanism in AR remains unclear. We aimed to identify a quercetin-related epithelial pathway involved in house dust mite (HDM)-induced nasal epithelial injury.
Methods:
Network pharmacology screened quercetin-related AR targets. Molecular docking and dynamics evaluated quercetin-ALOX5 binding potential. ALOX5 expression was examined in AR nasal mucosa and HDM-stimulated human nasal epithelial cells. ALOX5 knockdown, MitoTEMPO, zileuton, and LTB4 add-back were used to assess ALOX5/LTB4 signaling, mitochondrial oxidative stress, and epithelial barrier dysfunction.
Results:
Network pharmacology prioritized ALOX5 as a highly ranked AR-related target of quercetin. Docking and molecular dynamics analysis supported a stable binding potential between quercetin and ALOX5. ALOX5 expression was increased in AR nasal mucosa and positively associated with symptom severity. HDM induced ALOX5 expression in nasal epithelial cells. ALOX5 knockdown reduced HDM-induced mitochondrial ROS accumulation, restored mitochondrial membrane potential, and improved ATP production. Both ALOX5 knockdown and MitoTEMPO restored ZO-1 and E-cadherin expression under HDM stimulation. Quercetin reduced HDM-induced ALOX5 expression and LTB4 production, alleviated mitochondrial oxidative stress, and improved epithelial barrier marker expression, whereas LTB4 add-back weakened these effects.
Conclusion:
These findings suggest that an ALOX5-associated mitochondrial oxidative stress pathway contributes to HDM-induced nasal epithelial barrier dysfunction. Quercetin may protect epithelial barrier integrity in AR, at least partly by suppressing ALOX5/LTB4 signaling and mitochondrial oxidative injury.
