Department of Neonatology, Dr. Sami Ulus Maternity and Children Research and Training Hospital, University of Health Sciences, Ankara,Turkey.
Department of Neonatology, Republic of Turkey Ministry of Health, Ankara City Hospital, Ankara,Turkey.
Comb Chem High Throughput Screen. 2021;24(8):1243-1250. doi: 10.2174/1386207323666200915092012.
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).
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.
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).
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.
背景/目的：本研究旨在确定虾青素对高氧和脂多糖（LPS）诱导的支气管肺发育不良（BPD）大鼠肺的作用。
42 只新生 Wistar 大鼠，来自自发性妊娠大鼠，分为三组：高氧（95% O2）+脂多糖（LPS）组、高氧+LPS+虾青素组和对照组：无治疗组（21% O2）。高氧+LPS+虾青素组的幼仔从第一天到第五天每天给予 100mg/kg 口服虾青素。进行组织病理学和生化评估，包括谷胱甘肽（GSH）、总抗氧化状态（TAS）、总氧化状态（TOS）、脂质过氧化物（LPO）、8-羟基脱氧鸟苷（8-OHdG）、高级氧化蛋白产物（AOPP）、髓过氧化物酶（MPO）、总巯基、肿瘤坏死因子-α（TNF-α）、白细胞介素 1β（IL-1β）和 caspase-3 活性。
高氧+LPS+虾青素组的存活率和体重增加率均较高（p<0.001）。在组织病理学评估中，高氧+LPS+虾青素组的肺损伤严重程度明显减轻，凋亡减少（ELISA 法检测 caspase-3）（p<0.001）。肺组织的生化分析表明，与高氧+LPS 组相比，虾青素治疗组的 TAS、GSH 和总巯基水平显著升高（p<0.05），而 TOS、AOPP、LPO、8-OHdG 和 MPO 水平显著降低（p<0.001）。此外，与高氧+LPS 组相比，虾青素治疗组肺组织中的 TNF-α和 IL-1β水平显著降低（p<0.001）。
虾青素具有抗炎、抗氧化、抗凋亡作用，可减轻炎症和高氧引起的肺损伤，保护肺免受严重破坏。
