Alamandine Mitigates Inflammation and Oxidative Stress in OVA-Induced Asthma: A Novel Therapeutic Approach

Background: Asthma is a chronic inflammatory airway disease characterized by airway hyperresponsiveness, mucus overproduction, and oxidative stress. Alamandine (Ala), a peptide of the renin–angiotensin system, has shown anti-inflammatory and antioxidant properties in several experimental models. This study aimed to investigate the potential protective effects of Ala in an ovalbumin (OVA)-induced model of allergic asthma in mice. Methods: Thirty-five male mice were divided into control, OVA, OVA+Ala, OVA+dexamethasone, and Ala-only groups. Asthma was induced by sensitization and challenge with OVA. Ala (50 μg/kg) and dexamethasone (2 mg/kg) were administered intraperitoneally during the challenge phase. Lung tissues and serum samples were analyzed for inflammatory cytokines, oxidative stress markers, and histopathological alterations. Results: Treatment with Ala significantly reduced airway inflammation, eosinophil infiltration, and mucus secretion compared with the OVA group. Ala also downregulated the expression of pro-inflammatory cytokines (IL-6 and TNF-α) and suppressed NF-κB activation. Furthermore, oxidative stress markers improved following Ala administration, indicating its antioxidant potential. The effects of Ala were comparable, in part, to those of dexamethasone. Conclusion: These findings suggest that Ala may exert protective effects against allergic airway inflammation and oxidative stress in an OVA-induced asthma model. The observed improvements in cytokine levels and tissue pathology indicate that Ala could help modulate inflammatory signaling pathways involved in asthma. However, further experimental and clinical studies are needed to confirm these results and to clarify the underlying mechanisms of Ala’s action in asthma management.