Open Access

Regulation of the angiotensin II-p22phox-reactive oxygen species signaling pathway, apoptosis and 8-oxoguanine-DNA glycosylase 1 retrieval in hyperoxia-induced lung injury and fibrosis in rats

  • Authors:
    • Yu Wang
    • Yuxi Zhu
    • Yudi Zhu
    • Zhongyi Lu
    • Feng Xu
  • View Affiliations

  • Published online on: May 5, 2017     https://doi.org/10.3892/etm.2017.4429
  • Pages: 3397-3407
  • Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The present study was designed to explore the impact of hyperoxia on lung injury and fibrosis via the angiotensin II (AngII)-p22phox‑reactive oxygen species (ROS) signaling pathway, apoptosis and 8‑oxoguanine‑DNA glycosylase 1 (OGG1) repair enzyme. Newborn Sprague‑Dawley rats were randomly divided in the newborn air group, newborn hyperoxia group and newborn intervention group, the latter of which was administered the chymotrypsin inhibitor, 2-(5-formylamino-6-oxo-2-phenyl-1, 6‑dihydropyrimidine‑1‑yl)‑N‑[4‑dioxo‑1‑phenyl‑7‑(2‑pyridyloxy)]​2‑heptyl‑acetamide (NK3201). A group of adult rats also received hyperoxic treatment. Histomorphological changes in lung tissues were dynamically observed. AngII, ROS, angiotensin type 1 receptor (AT1R) and p22phox messenger RNA (mRNA) levels, and OGG1 and peroxisome proliferator‑activated receptor‑γ (PPARγ) protein levels in the lung tissues were detected at various times after hyperoxia. Hyperoxia led to traumatic changes in the lungs of newborn rats that resulted in decreased viability, increased mortality, morphological changes and the apoptosis of alveolar type II epithelial cells (AT‑II), as well as increased expression levels of AngII, AT1R and p22phox, which would ultimately lead to secondary diseases. NK3201 significantly inhibited the hyperoxia‑induced increased expression of AngII, AT1R and p22phox and further promoted OGG1 and PPARγ protein expression, thus reducing the intrapulmonary ROS level, the apoptotic index and caspase‑3 levels. However, the adult hyperoxia group only exhibited tachypnea and reduced viability. This study suggested that the AngII‑p22phox‑ROS signaling pathway, PPARγ and OGG1 together contributed to the hyperoxia‑induced lung injury and that NK3201 was able to reverse the effects of hyperoxia.

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June-2017
Volume 13 Issue 6

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Wang Y, Zhu Y, Zhu Y, Lu Z and Xu F: Regulation of the angiotensin II-p22phox-reactive oxygen species signaling pathway, apoptosis and 8-oxoguanine-DNA glycosylase 1 retrieval in hyperoxia-induced lung injury and fibrosis in rats. Exp Ther Med 13: 3397-3407, 2017
APA
Wang, Y., Zhu, Y., Zhu, Y., Lu, Z., & Xu, F. (2017). Regulation of the angiotensin II-p22phox-reactive oxygen species signaling pathway, apoptosis and 8-oxoguanine-DNA glycosylase 1 retrieval in hyperoxia-induced lung injury and fibrosis in rats. Experimental and Therapeutic Medicine, 13, 3397-3407. https://doi.org/10.3892/etm.2017.4429
MLA
Wang, Y., Zhu, Y., Zhu, Y., Lu, Z., Xu, F."Regulation of the angiotensin II-p22phox-reactive oxygen species signaling pathway, apoptosis and 8-oxoguanine-DNA glycosylase 1 retrieval in hyperoxia-induced lung injury and fibrosis in rats". Experimental and Therapeutic Medicine 13.6 (2017): 3397-3407.
Chicago
Wang, Y., Zhu, Y., Zhu, Y., Lu, Z., Xu, F."Regulation of the angiotensin II-p22phox-reactive oxygen species signaling pathway, apoptosis and 8-oxoguanine-DNA glycosylase 1 retrieval in hyperoxia-induced lung injury and fibrosis in rats". Experimental and Therapeutic Medicine 13, no. 6 (2017): 3397-3407. https://doi.org/10.3892/etm.2017.4429