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
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