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[Protection of captopril against chronic lung disease induced by hyperoxia in neonatal rats].
Zhongguo Dang Dai Er Ke Za Zhi. 2007 Apr; 9(2):169-73.ZD

Abstract

OBJECTIVE

This study examined the protein and mRNA contents of angiotesin converting enzyme (ACE), angiotensin II (Ang II) and type I collagen and the changes of lung histomorphology in neonatal rats with hyperoxia-induced chronic lung disease (CLD) and investigated the protection of captopril against CLD and the possible mechanism.

METHODS

A total of 240 term neonatal Wistar rats were randomly assigned into air, model, normal saline and captopril-treated groups (n=60 each). The air group was exposed to room air (FiO2=0.21) immediately after birth. The other three groups were exposed to hyperoxia (FiO2=0.9) for 21 days to induce lung injury. The captopril-treated group received captopril daily (30 mg/kg) by intragastric administration between the 7th and 21st days of hyperoxia exposure. The normal saline group was administrated with normal saline instead. At each time interval of 1, 3, 7, 14 and 21 days after experiment, six rats of each group were randomly chosen and sacrificed. The protein and mRNA levels of ACE, Ang II and type I collagen were measured by enzyme-linked immunosorbentassay, radio-immunity technique and RT-PCR. The changes of lung histomorphology were observed under a light microscope.

RESULTS

The protein and mRNA expressions of ACE, Ang II and type I collagen increased significantly in the model and normal saline groups on the 14th and peaked on the 21st days of exposure compared with those of the air group (P < 0.05 or 0.01). Captopril treatment reduced significantly the protein and mRNA expressions of ACE, Ang II and type I collagen compared the model and normal saline groups on the 14th and 21st days, although the values were significantly higher than the air group (P < 0.05). The histopathologic examination demonstrated broadened lung interstitium and reduced alveolar quantity and lung fibrosis was developed in the model and normal saline groups on the 14th day of exposure. Captopril treatment obviously alleviated the changes of lung histomorphology.

CONCLUSIONS

Captopril can inhibit the protein and mRNA expressions of ACE, Ang II and type I collagen and alleviate lung fibrosis in neonatal rats with hyperoxia-induced lung injury/CLD. This may contribute to one of the possible mechanisms underlying the protective effects of captopril against lung injury/CLD.

Authors+Show Affiliations

Department of Pediatrics, Second Affiliated Hospital, China Medical University, Shenyang, China. lijiujun@21cn.comNo affiliation info available

Pub Type(s)

English Abstract
Journal Article
Research Support, Non-U.S. Gov't

Language

chi

PubMed ID

17448318

Citation

Li, Jiu-Jun, and Xin-Dong Xue. "[Protection of Captopril Against Chronic Lung Disease Induced By Hyperoxia in Neonatal Rats]." Zhongguo Dang Dai Er Ke Za Zhi = Chinese Journal of Contemporary Pediatrics, vol. 9, no. 2, 2007, pp. 169-73.
Li JJ, Xue XD. [Protection of captopril against chronic lung disease induced by hyperoxia in neonatal rats]. Zhongguo Dang Dai Er Ke Za Zhi. 2007;9(2):169-73.
Li, J. J., & Xue, X. D. (2007). [Protection of captopril against chronic lung disease induced by hyperoxia in neonatal rats]. Zhongguo Dang Dai Er Ke Za Zhi = Chinese Journal of Contemporary Pediatrics, 9(2), 169-73.
Li JJ, Xue XD. [Protection of Captopril Against Chronic Lung Disease Induced By Hyperoxia in Neonatal Rats]. Zhongguo Dang Dai Er Ke Za Zhi. 2007;9(2):169-73. PubMed PMID: 17448318.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Protection of captopril against chronic lung disease induced by hyperoxia in neonatal rats]. AU - Li,Jiu-Jun, AU - Xue,Xin-Dong, PY - 2007/4/24/pubmed PY - 2007/5/12/medline PY - 2007/4/24/entrez SP - 169 EP - 73 JF - Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics JO - Zhongguo Dang Dai Er Ke Za Zhi VL - 9 IS - 2 N2 - OBJECTIVE: This study examined the protein and mRNA contents of angiotesin converting enzyme (ACE), angiotensin II (Ang II) and type I collagen and the changes of lung histomorphology in neonatal rats with hyperoxia-induced chronic lung disease (CLD) and investigated the protection of captopril against CLD and the possible mechanism. METHODS: A total of 240 term neonatal Wistar rats were randomly assigned into air, model, normal saline and captopril-treated groups (n=60 each). The air group was exposed to room air (FiO2=0.21) immediately after birth. The other three groups were exposed to hyperoxia (FiO2=0.9) for 21 days to induce lung injury. The captopril-treated group received captopril daily (30 mg/kg) by intragastric administration between the 7th and 21st days of hyperoxia exposure. The normal saline group was administrated with normal saline instead. At each time interval of 1, 3, 7, 14 and 21 days after experiment, six rats of each group were randomly chosen and sacrificed. The protein and mRNA levels of ACE, Ang II and type I collagen were measured by enzyme-linked immunosorbentassay, radio-immunity technique and RT-PCR. The changes of lung histomorphology were observed under a light microscope. RESULTS: The protein and mRNA expressions of ACE, Ang II and type I collagen increased significantly in the model and normal saline groups on the 14th and peaked on the 21st days of exposure compared with those of the air group (P < 0.05 or 0.01). Captopril treatment reduced significantly the protein and mRNA expressions of ACE, Ang II and type I collagen compared the model and normal saline groups on the 14th and 21st days, although the values were significantly higher than the air group (P < 0.05). The histopathologic examination demonstrated broadened lung interstitium and reduced alveolar quantity and lung fibrosis was developed in the model and normal saline groups on the 14th day of exposure. Captopril treatment obviously alleviated the changes of lung histomorphology. CONCLUSIONS: Captopril can inhibit the protein and mRNA expressions of ACE, Ang II and type I collagen and alleviate lung fibrosis in neonatal rats with hyperoxia-induced lung injury/CLD. This may contribute to one of the possible mechanisms underlying the protective effects of captopril against lung injury/CLD. SN - 1008-8830 UR - https://www.unboundmedicine.com/medline/citation/17448318/[Protection_of_captopril_against_chronic_lung_disease_induced_by_hyperoxia_in_neonatal_rats]_ L2 - https://medlineplus.gov/lungdiseases.html DB - PRIME DP - Unbound Medicine ER -