Effects of Aerobic Exercise and Carvacrol Supplementation on NRF2/NF-κB Signaling Pathway in an Ovalbumin-Induced Allergic Asthma Model in Rats

Background:Allergic asthma is a chronic inflammatory airway disease characterized by excessive oxidative stress, persistent inflammation, and structural remodeling of lung tissue.The nuclear factor erythroid 2-related factor 2 (NRF2) and nuclear factor kappa B (NF-κB) signaling pathways play key roles in regulating antioxidant defense and inflammatory responses, respectively. This study aimed to evaluate the effects of aerobic exercise and carvacrol supplementation, alone and in combination, on oxidative stress markers, respiratory function, lung remodeling, and NRF2/NF-κB signaling in an ovalbumin-induced allergic asthma model in rats. Methods:Male Wistar rats were randomly assigned to control, allergic asthma, asthma+aerobic exercise, asthma+carvacrol, and asthma+aerobic exercise+carvacrol groups (n=8/group). Lung tissue was analyzed for TAC, SOD activity, malondialdehyde levels, hydroxyproline content, and protein expression of NRF2 and NF-κB. Respiratory rate was also assessed. Results: Asthmatic rats showed significantly increased oxidative stress, elevated NF-κB expression, higher respiratory rate, and increased lung hydroxyproline content, along with reduced antioxidant enzyme activities and NRF2 expression compared with controls (P < 0.001). Aerobic exercise or carvacrol treatment significantly improved antioxidant status, reduced MDA levels, suppressed NF-κB expression, and attenuated lung remodeling (P < 0.05–0.01). The combined exercise and carvacrol intervention produced the greatest protective effects, markedly enhancing NRF2 expression while further inhibiting NF-κB signaling and improving respiratory and structural outcomes (P < 0.001 vs. asthma). Conclusion: In this preclinical allergic asthma model, aerobic exercise combined with carvacrol supplementation showed greater protective effects than either intervention alone, probably by improving antioxidant defenses and attenuating NF-κB-mediated inflammatory signaling through modulation of the NRF2/NF-κB pathway.