Melatonin attenuates inflammation, remodeling, and oxidative stress in experimental models of asthma and COPD.
Asthma and chronic obstructive pulmonary disease (COPD) are characterized by persistent airway inflammation, oxidative stress, and structural remodeling, leading to progressive impairment of lung function. Melatonin has anti-inflammatory and antioxidant properties and may represent a promising therapeutic strategy for chronic airway diseases.
To evaluate the therapeutic effects of melatonin on airway hyperresponsiveness, inflammation, oxidative stress, and remodeling in experimental models of asthma and COPD.
Forty male BALB/c mice were allocated into five groups (n = 8/group): SAL, OVA, OVA+MEL, ELA, and ELA+MEL. Asthma and emphysema were induced by ovalbumin and elastase, respectively. Melatonin (15 mg/kg, intraperitoneally) was administered from days 22 to 27. Respiratory mechanics, bronchoalveolar lavage fluid, immunohistochemistry, and gene expression analyses were performed to evaluate inflammatory cytokines, remodeling markers, and oxidative stress-related proteins.
Melatonin significantly attenuated airway hyperresponsiveness in the asthma model, reducing respiratory mechanical parameters, inflammatory cell infiltration, and eosinophilia. In both asthma and emphysema models, melatonin markedly decreased the expression of pro-inflammatory cytokines, remodeling markers (MMP-9, MMP-12, TIMP-1, and TGF-β), and oxidative stress-related mediators (NF-κB and iNOS). These findings were further supported by gene expression analyses, demonstrating broad suppression of inflammatory cytokines following treatment.
Melatonin attenuated inflammation, oxidative stress, and airway remodeling while improving lung function, particularly in experimental asthma. These findings highlight melatonin as a promising adjunctive therapeutic strategy for chronic inflammatory lung diseases by simultaneously targeting multiple pathogenic pathways.
To evaluate the therapeutic effects of melatonin on airway hyperresponsiveness, inflammation, oxidative stress, and remodeling in experimental models of asthma and COPD.
Forty male BALB/c mice were allocated into five groups (n = 8/group): SAL, OVA, OVA+MEL, ELA, and ELA+MEL. Asthma and emphysema were induced by ovalbumin and elastase, respectively. Melatonin (15 mg/kg, intraperitoneally) was administered from days 22 to 27. Respiratory mechanics, bronchoalveolar lavage fluid, immunohistochemistry, and gene expression analyses were performed to evaluate inflammatory cytokines, remodeling markers, and oxidative stress-related proteins.
Melatonin significantly attenuated airway hyperresponsiveness in the asthma model, reducing respiratory mechanical parameters, inflammatory cell infiltration, and eosinophilia. In both asthma and emphysema models, melatonin markedly decreased the expression of pro-inflammatory cytokines, remodeling markers (MMP-9, MMP-12, TIMP-1, and TGF-β), and oxidative stress-related mediators (NF-κB and iNOS). These findings were further supported by gene expression analyses, demonstrating broad suppression of inflammatory cytokines following treatment.
Melatonin attenuated inflammation, oxidative stress, and airway remodeling while improving lung function, particularly in experimental asthma. These findings highlight melatonin as a promising adjunctive therapeutic strategy for chronic inflammatory lung diseases by simultaneously targeting multiple pathogenic pathways.
Authors
Ribeiro Ribeiro, João João, de Almeida de Almeida, Fukuzaki Fukuzaki, Bezerra Bezerra, Scheffer Scheffer, Roberto Roberto, Santos Zambon Robertoni Santos Zambon Robertoni, da Silva da Silva, Teodoro Teodoro, Righetti Righetti, Camargo Camargo, Tibério Tibério, Leick Leick
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