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Lycopene mitigates pulmonary emphysema induced by cigarette smoke in a murine model
- Campos, Keila Karine Duarte, de Oliveira Ramos, Camila, Martins, Thais Lourenço, Costa, Guilherme de Paula, Talvani, André, Garcia, Camila Carrião Machado, Oliveira, Laser Antônio Machado, Cangussú, Sílvia Dantas, Costa, Daniela Caldeira, Bezerra, Frank Silva
- The Journal of nutritional biochemistry 2019 v.65 pp. 93-100
- DNA damage, air flow, animal models, anti-inflammatory activity, anti-inflammatory agents, antioxidants, bronchitis, catalase, inflammation, interferon-gamma, interleukin-10, leukocytes, lipid peroxidation, lungs, lycopene, mice, nitrites, pulmonary emphysema, sunflower oil, superoxide dismutase, tumor necrosis factor-alpha
- Chronic obstructive pulmonary disease (COPD) is an inflammatory lung disease characterized by a non-fully reversible airflow limitation comprising chronic bronchitis and pulmonary emphysema both being induced by cigarette smoke (CS) exposure. Lycopene has shown antioxidant and anti-inflammatory properties that can prevent acute lung inflammation and emphysema. We hypothesized that administration with lycopene would repair lung damage in emphysema caused by CS exposure. Mice were administered with two different doses of lycopene (25 or 50 mg/kg/day, diluted in sunflower oil by orogastric gavage) and then exposed to 60 days of CS or not (CG). Lycopene promoted a reduction in the number of total leukocytes and it improved pulmonary emphysema. Lycopene was able to minimize redox processes by decreasing lipid peroxidation and DNA damage, and by having an increase in the activities of SOD, CAT and GSH content. Furthermore, it decreased levels of TNF-α, IFN-γ and IL-10. In addition, it was able to decrease MPO activity and nitrite content. In conclusion, our data elucidated the role of lycopene as an antioxidant and anti-inflammatory agent in mice exposed to CS.