Open Access

Establishment and evaluation of a simulated high‑altitude hypoxic brain injury model in SD rats

  • Authors:
    • Ya Hou
    • Xiaobo Wang
    • Xiaorui Chen
    • Jing Zhang
    • Xiaopeng Ai
    • Yusheng Liang
    • Yangyang Yu
    • Yi Zhang
    • Xianli Meng
    • Tingting Kuang
    • Yao Hu
  • View Affiliations

  • Published online on: February 5, 2019     https://doi.org/10.3892/mmr.2019.9939
  • Pages: 2758-2766
  • Copyright: © Hou et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

This study was conducted to establish a stable hypobaric hypoxia brain injury model. SD rats were randomly separated into control and model groups, and placed outside or inside of a hypobaric chamber, respectively. Subsequent to 24 h anoxic exposure, plasma superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), oxidized glutathione (GSSG) and lactate dehydrogenase (LDH) were measured using commercial biochemical kits. Hematoxylin‑eosin (H&E), Nissl's and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining were used to observe the morphology of neurons in the hippocampus. The protein expression levels of apoptotic protease activating factor‑1 (Apaf‑1), hypoxia inducible factor‑1α (HIF‑1α), caspase‑3, cleaved caspase‑3, Bcl‑2‑associated X protein (Bax) and cytochrome c (cyto‑c) were detected using western blot and immunohistochemistry analyses. Hypoxic substantially induced morphological lesions in the hippocampus concomitant with the physical behavioral performance deficit. Furthermore, hypoxia markedly exacerbated the levels of MDA, LDH and GSSG, and restrained GSH (P<0.01) and SOD (P<0.05) levels compared with the control group. In addition, hypoxia significantly induced the protein expression of Apaf‑1, HIF‑1α, caspase‑3, cleaved caspase‑3, Bax and Cyto‑c (P<0.01) compared with the control group. Finally, a lower number and volume of Nissl bodies were verified in the hypoxic group. TUNEL results demonstrated a greater number of apoptotic cells in the hypoxic group. The present study demonstrates a model of rat hypoxic brain injuries induced by a hypobaric chamber at 9,000 m for 24 h. Furthermore, the redox enzyme, HIF‑1α and mitochondrial apoptosis‑associated protein, along with H&E and Nissl's staining, may be applied to evaluate the degree of injury.
View Figures
View References

Related Articles

Journal Cover

April-2019
Volume 19 Issue 4

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Hou Y, Wang X, Chen X, Zhang J, Ai X, Liang Y, Yu Y, Zhang Y, Meng X, Kuang T, Kuang T, et al: Establishment and evaluation of a simulated high‑altitude hypoxic brain injury model in SD rats. Mol Med Rep 19: 2758-2766, 2019.
APA
Hou, Y., Wang, X., Chen, X., Zhang, J., Ai, X., Liang, Y. ... Hu, Y. (2019). Establishment and evaluation of a simulated high‑altitude hypoxic brain injury model in SD rats. Molecular Medicine Reports, 19, 2758-2766. https://doi.org/10.3892/mmr.2019.9939
MLA
Hou, Y., Wang, X., Chen, X., Zhang, J., Ai, X., Liang, Y., Yu, Y., Zhang, Y., Meng, X., Kuang, T., Hu, Y."Establishment and evaluation of a simulated high‑altitude hypoxic brain injury model in SD rats". Molecular Medicine Reports 19.4 (2019): 2758-2766.
Chicago
Hou, Y., Wang, X., Chen, X., Zhang, J., Ai, X., Liang, Y., Yu, Y., Zhang, Y., Meng, X., Kuang, T., Hu, Y."Establishment and evaluation of a simulated high‑altitude hypoxic brain injury model in SD rats". Molecular Medicine Reports 19, no. 4 (2019): 2758-2766. https://doi.org/10.3892/mmr.2019.9939