Protect effects of Captopril on neonatal Wistar rats with lung fibrosis induced by hyperoxia / 中国小儿急救医学

ABSTRACT

Objective To observe the dynamic changes and the effects of Captopril on interstitial fibrosis in lung tissue of neonatal rats with lung fibrosis induced by hyperoxia. Methods Two hundred and forty neonatal Wistar rats were randomly assigned into model group, air control group, normal saline control and Captopril-trcated group (n=60 each).The air control group was exposed to room air (FiO2 = 0.21), and the rest three groups were continuously exposed to hyperoxia (FiO2 = 0.9) for 21 days. During the exposure, the Captopril-treated group received Captopril [ 30 mg/( kg·d) ] by intragastric administration, and the normal saline control group was administrated with normal saline instead, the model group did not receive any treatment. On the 1 st, 3 rd, 7 th, 14 th and 21 st day of exposure, the subjects were sacrificed. And then, the protein levels of collagen Ⅲ (Co-Ⅲ ) were measured by enzyme-linked immunosorbent assay and angiotensin Ⅱ(Ang Ⅱ )by radio-immunity technique, and the mRNA expression of Ang Ⅱ, Co- Ⅲ was measured by RT-polymerase chain reaction. The changes of lung histomorphology were observed. Results On the 14 th day, The Ang Ⅱ, Co- Ⅲ protein levels and their mRNA expression of modal group and normal saline control group increased significantly as compared to the air control group ( P < 0.05 ), except the Ang Ⅱ mRNA expression of normal saline control group. The Ang Ⅱ and Co-Ⅲ protein levels of model group was (838.22 ± 197.75 ) and ( 104.21 ± 43.37) ng/mg respectively, and normal saline control group was ( 759.97 ± 60.81 ) and ( 128.69 ± 54.74) ng/mg respectively on the 21 st day, their mRNA expression of two groups also increased to the peak on the 21 st day(P< 0.05).The AnglI and Co- Ⅲ protein levels of Captopril-treated group was (554.52 ± 59.32) and (39.90 ± 13.45) ng/mg on the 21 st day respectively, their mRNA expression was (1.50 ± 0.84 ) and (1.13 ± 0.55) respectively, and decreased significantly as compared to the model group and normal saline control group respectively (P<0.05), but increased significantly as campared to the air control group (P < 0.05). The histopathological examination demonstrated different degrees of alveolitis, broaden interstitium and reduced alveolar quantity in the model group and normal saline control group compared with air control group. The pathological changes were markedly alleviated in the Captopril-treated group. Conclusion Captopril may have protective effects on lung injury induced by hyperoxia.