Purpose The purpose of this study was to evaluate the preventive effect of CDP-choline treatment on hyperoxic lung injury, inflammation and apoptosis in a neonatal rat model of bronchopulmonary dysplasia BPD.
Methods A total of 30 newborn pups were arranged in control, hyperoxia, and hyperoxia+CDP-choline groups. Immediately after birth, pups in the control group were kept in room air containing 21% O2 and received daily saline injections, while those in hyperoxia and hyperoxia+CDP-choline groups were exposed to 95% O2 and received daily injections of saline and CDP-choline (300 mg/kg), respectively, throughout postnatal day 10 (P10). Histopathological scoring, radial alveolar count, lamellar body protein expression, fibrosis, proinflammatory cytokine levels, oxidant/antioxidant enzyme activities, malondialdehyde content and apoptosis were evaluated on lung samples obtained at P10.
Results Hyperoxia induced severe lung damage as evidenced by cell infiltration, edema and fibrosis which were reduced significantly by CDP-choline treatment. Radial alveolar count and lamellar body protein expression were significantly recovered, while number of TUNEL-positive cells and active Caspase-3 expression were decreased by CDP-choline administration. Tissue proinflammatory cytokine (IL-1b, IL-6 and TNF-α) levels as well as tissue MDA content and MPO activities were reduced, whereas GSH-Px and SOD activities were preserved in hyperoxia+CDP-choline group.
Conclusions Our data show for the first time that parenteral CDP-choline administration prevents hyperoxic lung injury in a neonatal rat model of BPD. It may therefore be suggested that CDP-choline can be used as an effective therapeutic agent for prevention of BPD in case it exhibits similar effects in humans.
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