Anti-inflammatory and protective effects of D-carvone on lipopolysaccharide (LPS)-induced acute lung injury in mice

Abstract

Lung inflammation is a common cause of health problem and death among adults and children. Antioxidant compounds have the capability to overcome this complication. This study targets to examine the anti-inflammatory and defensive role of D-carvone on lipopolysaccharide (LPS)-initiated lung damage in mice. Male BALB/c mice (n = 8) received intragastric feeding of D-carvone (25 and 50 mg/kg b.w.) or dexamethasone (5 mg/kg b.w.) an hour before intranasal instillation of LPS (20 µg). Seven hours after LPS instillation, the bronchoalveolar lavage fluid (BALF), blood serum, and tissue samples of lung were studied for the levels of inflammatory cells, antioxidant enzymes, pro-inflammatory cytokines, and histopathological changes. D-carvone significantly alleviated (p < 0.05) the lung damage caused by LPS by reducing the lung wet-to-dry (W/D) ratio along with the amount of total cells, macrophages, and neutrophils in BALF (p < 0.05). The serum TNF-α, IL-1β, and IL-6 were remarkably reduced (p < 0.05) in D-carvone treated mice. Histopathological derangements because of LPS-initiated lung damage were altered by D-carvone. The results of D-carvone were comparable with the positive control dexamethasone. Pre-treatment of D-carvone significantly provided anti-inflammatory and protective effect in LPS-instigated lung damage. Together, these findings acknowledge the use of D-carvone as preventive agent for lung damage and inflammation. Further research on the pharmacokinetics, pathway and mechanism of action of D-carvone are necessary to promote D-carvone as a commercial anti-inflammatory drug.