Objective To determine the effect of prolonged hyperoxia on neonatal rat lung. Methods Full term and premature newborn SD rats were continuosly exposed to 85% oxygen or room air 7 and 14 days after birth.The activities of 3 different kinds of antioxidant enzyme (AOE) including superoxide dismutase(SOD), glutathion peroxidase (GP) and catalase (CAT) in supernatant fractions of lung homogenates were assessed after 7 and 14 days of exposure. So was the lung hydroproline content. Results (1)AOE acctivitis: Except CAT activity at 14 days of exposure, others AOE activities in O 2 exposed rat pups were significantly higher than those in air exposed controls (P

Objective:To investigate the effects of different concentrations of hydrogen peroxide (H 2O 2) on the expression of histone deacetylase-2(HDAC-2) and mitogen activated protein kinases phosphatases-1(MKP-1) in A549 cells. Methods:The experimental models of A549 cells were established by intervening of different concentrations of H 2O 2(0, 100, 200, 400, 600, 800 μmol/L)for 2 h, 4 h, 8 h, 12 h and 24 h, respectively.The survival rate of A549 cells was detected by thiazolyl blue(MTT) assay, and the apoptosis of A549 cells was tested by lactic dehydrogenase(LDH) assay.The expression of HDAC-2 and MKP-1 protein was detected by Western blot. Results:(1)MTT results showed that compared with the control group (H 2O 2 was 0 μmol/L), the survival rate of A549 cells was decreased with the increase of H 2O 2 concentration at 2 h, 4 h, 8 h, 12 h, 24 h and 48 h. (2)LDH results showed that, compared with the control group, the inhibition rate of A549 cells increased with the increase of H 2O 2 concentration at 2 h, 4 h, 8 h, 12 h, 24 h and 48 h. (3)The expression of HDAC-2 protein decreased ( F=14.588, P<0.01), and the expression of MKP-1 protein increased ( F=64.297, P<0.01) in a concentration-dependent manner with the increase of H 2O 2 concentration at 12 h after H 2O 2 treatment. Conclusions:H 2O 2 participates in oxidative stress injury of lung cells by regulating the expression of HDAC-2 and MKP-1.

Bronchopulmonary dysplasia (BPD) is a common chronic respiratory complication in preterm infants without fully understand the mechanism or effective treatment, which could significantly affect the survival rate and prognosis of these infants. Studies have confirmed that epigenetic mechanisms, including histone modification, non-coding RNA and DNA methylation may play an essential role in the onset and development of BPD. And most related epigenetic changes are reversible, which might serve as a potential target for BPD treatment. Therefore, further studies on epigenetics will shed light on a better understanding of the pathogenesis, prevention, and treatment of BPD.