Abstract
Smoke inhalation damage defined as mucosal damage in the respiratory system caused by flames, hot air, steam, toxic gas and particulate matter in smoke. Oxidative stress is an important mechanism, as high temperature smoke contains a high concentration of strong oxidants. The resultant inflammatory response, if uncontrolled, causes abundant inflammatory cell accumula-tion in the lungs, producing excessive reactive oxygen species (ROS) and inducing oxidative stress injury. A total of forty adult male Sprague-Dawley albino rats were used. Sham group (n:8) was kept in smoke study room for 28 min without giving any injury and treatment. Control group (n:8); the dorsum of rats was shaved and surgically scrubbed. After receiving 30% burn injury they received four series of smoke and four series of 100% oxygen between smoke inhalations. ASX groups; after receiving 30% burn injury the same inhalation injury protocol was applied to these groups. After exposure to smoke and burn injury, ASX10 (n:8) animals received 10 mg/kg/d astaxanthin, ASX30 (n:8) animals received 30 mg/kg/d astaxanthin, ASX100 (n:8) animals received 100 mg/kg/d astaxanthin dissolved in 5ml of olive oil for 3 days with orogastric route. For histopathologic examination, samples were taken from trachea, and mid-portion of parenchyma. For biochemical analysis, samples taken from the right lower lobes and stored at –80 °C. Histologic assessment of alveolar congestion and neutrophilic infiltration were statistically increased in group control than ASX10, ASX30 and ASX100 groups. Histologic assessment of haemorrhage and alveolar wall thickness was increased in group control than ASX30 and ASX100 groups. 4-HNE and NF-кβ levels in control group was significantly increased than ASX10, ASX30 and ASX100 groups. Proinflammatory cytokines TNF-α, IL-6 and IL-1β levels in lung tissue decreased by astaxanthin treatment at doses of 30mg/kg/d and 100mg/kg/d (p<0,05). Oxidative stress marker MDA levels and GR levels in lung tissue decreased by astaxanthin treatment (p<0,05). Our results have demonstrated that astaxanthin use have a beneficial role in smoke inhalation injury accompanying 30% tbsa burn of rats. Thus, astaxanthin may represent a potential approach to prevent systemic response due to oxidative stress and inflammatory processes of smoke inhalation injury and >30% burns.