Hasan Akduman*, Cüneyt Tayman, Ufuk Çakir, Esra Çakir, Dilek Dilli, Tuğba Taşkin Türkmenoğlu and Ataman Gönel Pages 1243 - 1250 ( 8 )
Background/Aim: This study aimed to ascertain the effects of astaxanthin on the lungs of rat pups with bronchopulmonary dysplasia (BPD) induced by hyperoxia and lipopolysaccharide (LPS).Materials and Methods: Forty-two newborn Wistar rats, born to spontaneous pregnant rats, were divided into three groups: Hyperoxia (95% O2) + lipopolysaccharide (LPS) group, hyperoxia + LPS + astaxhantin group, and control: no treatment group (21% O2). Pups in the hyperoxia + LPS + astaxanthin group were given 100 mg/kg/day oral astaxanthin from the first day to the fifth day. Histopathologic and biochemical evaluations, including glutathione (GSH), total anti-oxidant status (TAS), total oxidant status (TOS), lipid hydroperoxide (LPO), 8-hydroxydeoxyguanosine (8-OHdG), advanced oxidation protein products (AOPP), myeloperoxidase (MPO), total thiol, tumor necrosis factor-alpha (TNF-α), interleukin 1 beta (IL-1β), and caspase-3 activities, were performed. Results: Better survival rates and weight gain were demonstrated in the hyperoxia + LPS + astaxanthin group (p <0.001). In the histopathologic evaluation, the severity of lung damage was significantly reduced in the hyperoxia+LPS+astaxanthin group, as well as decreased apoptosis (ELİSA for caspase-3) (p <0.001). The biochemical analyses of lung tissues showed that TAS, GSH, and Total thiol levels were significantly higher in the astaxanthin treated group compared to the hyperoxia + LPS group (p <0.05) while TOS, AOPP, LPO, 8-OHdG, MPO levels were significantly lower (p <0.001). In addition, unlike the hyperoxia + LPS group, TNF-α and IL-1β levels in lung tissue were significantly lower in the astaxanthin-treated group (p <0.001). Conclusion: Astaxanthin was shown to reduce lung damage caused by inflammation and hyperoxia with its anti-inflammatory, anti-oxidant, anti-apoptotic properties, and to protect the lung from severe destruction.
Astaxanthin, bronchopulmonary dysplasia, rat, preterm birth, supplemental oxygen, respiratory morbidity.
Department of Neonatology, Dr. Sami Ulus Maternity and Children Research and Training Hospital, University of Health Sciences, Ankara, Department of Neonatology, Republic of Turkey Ministry of Health, Ankara City Hospital, Ankara, Department of Neonatology, Republic of Turkey Ministry of Health, Ankara City Hospital, Ankara, Department Anesthesiology and Clinical of Critical Care, Republic of Turkey Ministry of Health, Ankara City Hospital, Ankara, Department of Neonatology, Dr. Sami Ulus Maternity and Children Research and Training Hospital, University of Health Sciences, Ankara, Department of Pathology, Ministry of Health Dışkapı Yıldırım Beyazıt Training and Research Hospital, Ankara, Department of Medicinal Biochemistry, Medical Faculty, Harran University, Sanliurfa