Expression of heme oxygenase-1 and inducible nitric oxide synthase in the lungs of hyperoxia-exposed preterm rats

QUAN Yu-Feng, ZHENG Ming-Ci, ZHANG Hua, ZHANG Pei-Lin, ZHANG Hong

Chinese Journal of Contemporary Pediatrics ›› 2011, Vol. 13 ›› Issue (7) : 577-580.

PDF(1236 KB)
PDF(1236 KB)
Chinese Journal of Contemporary Pediatrics ›› 2011, Vol. 13 ›› Issue (7) : 577-580.
EXPERIMENTAL RESEARCH

Expression of heme oxygenase-1 and inducible nitric oxide synthase in the lungs of hyperoxia-exposed preterm rats

  • QUAN Yu-Feng, ZHENG Ming-Ci, ZHANG Hua, ZHANG Pei-Lin, ZHANG Hong
Author information +
History +

Abstract

OBJECTIVE: To study the expression and the role of heme oxygenase-1 (HO-1) and inducible nitric oxide synthase (iNOS) in preterm rats with hyperoxia-induced lung injuries. METHODS: Sixty-four three-day-old preterm Sprague-Dawley rats were randomly assigned to a hyperoxia group (90% oxygen exposure) and a control group (room air exposure), with 32 rats in each group. After 3 days or 7 days of exposure, the lung activity of HO-1 and nitric oxide (NO) contents in bronchoalveolar lavage fluid (BALF), pulmonary histopathologic changes, and the cellular distribution and expression of HO-1 and iNOS in the lungs were measured. RESULTS: After 3 days and 7 days of exposure, the hyperoxia group showed acute lung injuries characterized by the presence of hyperaemia, red cell extravasation and inflammatory infiltration. The NO contents in BALF and the iNOS expression in the lungs increased significantly in the hyperoxia group compared with those in the control group 3 and 7 days after exposure. The expression of HO-1 in macrophages in the lungs increased significantly in the hyperoxia group compared with that in the control group 3 and 7 days after exposure. The NO contents in BALF and the iNOS and HO-1 expression in the lungs increased significantly 7 days after hyperoxia exposure compared with 3 days after hyperoxia exposure. CONCLUSIONS: iNOS and HO-1 levels in the lungs increase in preterm rats with hyperoxia-induced lung injuries, suggesting that iNOS and HO-1 may play roles in hyperoxia-induced pulmonary injuries.

Key words

Heme oxygenase-1 / Inducible nitric oxide synthase / Hyperoxia / Lung / Preterm rats

Cite this article

Download Citations
QUAN Yu-Feng, ZHENG Ming-Ci, ZHANG Hua, ZHANG Pei-Lin, ZHANG Hong. Expression of heme oxygenase-1 and inducible nitric oxide synthase in the lungs of hyperoxia-exposed preterm rats[J]. Chinese Journal of Contemporary Pediatrics. 2011, 13(7): 577-580

References

[1]Farkas I, Maróti Z, Katona M, Endreffy E, Monostori P, Máder K, et al. Increased heme oxygenase-1 expression in premature infants with respiratory distress syndrome [J]. Eur J Pediatr, 2008, 167(12):1379-1383.

[2]Dennery PA, Rodgers PA, Lum MA, Jennings BC, Shokoohi V. Hyperoxic regulation of lung heme oxygenase in neonatal rats [J]. Pediatr Res, 1996, 40(6): 815-821.

[3]Ito Y, Betsuyaku T, Moriyama C, Nasuhara Y, Nishimura M. Aging affects lipopolysaccharide-induced upregulation of heme oxygenase-1 in the lungs and alveolar macrophages[J]. Biogerontology, 2009, 10(2): 173-180 .

[4]Pascal T, Debacq-Chainiaux F, Boilan E, Ninane N, Raes M, Toussaint O. Heme oxygenase-1 and interleukin-11 are overexpressed in stress-induced premature senescence of human WI-38 fibroblasts induced by tert-butylhydroperoxide and ethanol[J]. Biogerontology, 2007, 8(4): 409-422.

[5]全裕凤,郑明慈,张华,邓毅,张红.高体积分数氧暴露早产大鼠肺组织血红素加氧酶-1的表达及活性变化 [J] . 实用儿科临床杂志,2009,4(6):428-430.

[6]全裕凤,郑明慈,张华,张培林,张红.血红素氧合酶-1抑制剂锌原卟啉对早产鼠高氧肺损伤的影响 [J] . 实用儿科临床杂志,2009,24(18): 1409-1411.

[7]戎小平,邵勤,郭秀霞,江莲. 足月小于胎龄儿脐血中血红素氧合酶-1的测定及其在脐血管上的表达 [J]. 中国实用儿科杂志,2008,23(1):21-24.

[8]Chen W, Jia Z, Zhu H, Li Y, Misra HP. Ethyl pyruvate inhibits peroxynitrite-induced DNA damage and hydroxyl radical generation: implications for neuroprotection[J]. Neurochem Res, 2010, 35(2): 336-342.

[9]张向峰,梁瑛.高氧所致小鼠急性肺损伤时一氧化氮合成酶的表达(英文) [J]. 中华急诊医学杂志,2004,13(6):365-367.

[10]Auten RL, Mason SN, Whorton MH, Lampe WR, Foster WM, Goldberg RN, et al. Inhaled  ethyl nitrite prevents hyperoxia-impaired  postnatal alveolar development in newborn rats [J]. Am J Res Crti Car Med, 2007, 176(3): 291-299.

[11]Suttner DM, Sridhar K, Lee CS. Protective effects of transient HO-1 overexpressionon susceptibility to oxygen toxicity in lung cells[J]. Am J Physiol, 1999, 276(3 Pt 1): 443-448.

[12]Suttner DM, Dennery PA. Reversal of HO-1 related cytoprotection with increased expression is due to reactive iron[J]. FASEB J ,1999,13(13):1800-1805.

[13]张帆,夏中元,欧阳静萍.肠缺血再灌注致肺损伤时肺内HO-1/CO与 iNOS/NO 相互作用的研究[J].中国急救医学,2005,25(10) :728-730.

[14]Yang NC, Lu LH, Kao YH, Chau LY. Heme oxygenase-1 attenuates interleukin-1β-induced nitric oxide synthase expression in vascular smooth muscle cells [J].Biomed Sci, 2004, 11(6): 799-809.

[15]吕勇,孙波.吸入一氧化氮对儿科患者高铁血红蛋白浓度的影响[J].中国当代儿科杂志,2008,10(2):257-258.

[16]Siow RC, Sato H, Mann GE. Heme oxygenase-carbon monoxide signaling pathway in atherosclerosis: anti-atherogenic actions of bilirubin and carbon monoxide[J].Cardiovasc Res, 1999, 41(2): 385-390.
PDF(1236 KB)

Accesses

Citation

Detail

Sections
Recommended

/