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Molecular Medicine Reports
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Print ISSN: 1791-2997 Online ISSN: 1791-3004
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October-2017 Volume 16 Issue 4

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Article Open Access

Hydrogen saline suppresses neuronal cell apoptosis and inhibits the p38 mitogen‑activated protein kinase‑caspase‑3 signaling pathway following cerebral ischemia‑reperfusion injury

  • Authors:
    • Da Li
    • Yanqiu Ai

  • View Affiliations / Copyright

    Affiliations: Department of Anesthesiology, First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China
    Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 5321-5325
    |
    Published online on: August 21, 2017
       https://doi.org/10.3892/mmr.2017.7294
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Abstract

Cerebral ischemia‑reperfusion injury (CIRI) is a serious pathological disease that is associated with a high rate death and disability. Saturated hydrogen (H2) saline exhibits brain protective functions through anti‑inflammatory, antioxidant and antiapoptotic effects. The present study investigated the potential treatment effects of H2 on CIRI. In addition, the potential protective mechanisms of H2 in the prevention of CIRI were investigated. Adult, male Sprague‑Dawley rats (n=60) were randomly divided into the following three groups: Sham‑operated group; IR group; and IR + H2 group (0.6 mmol/l, 0.5 ml/kg/day). Hematoxylin and eosin, and TUNEL staining were performed for histopathological analysis and investigation of apoptosis, respectively. In addition, the protein expression of caspase‑3, p38 mitogen‑activated protein kinase (MAPK) and phosphorylated‑p38 MAPK in the cortex were measured by western blotting analysis. These results demonstrated that H2 significantly reduced the number of apoptotic cells, and the protein expression of p38 MAPK and caspase‑3, compared with the IR group. These effects may be associated with the p38MAPK signaling pathway.

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Copy and paste a formatted citation
Spandidos Publications style
Li D and Ai Y: Hydrogen saline suppresses neuronal cell apoptosis and inhibits the p38 mitogen‑activated protein kinase‑caspase‑3 signaling pathway following cerebral ischemia‑reperfusion injury. Mol Med Rep 16: 5321-5325, 2017.
APA
Li, D., & Ai, Y. (2017). Hydrogen saline suppresses neuronal cell apoptosis and inhibits the p38 mitogen‑activated protein kinase‑caspase‑3 signaling pathway following cerebral ischemia‑reperfusion injury. Molecular Medicine Reports, 16, 5321-5325. https://doi.org/10.3892/mmr.2017.7294
MLA
Li, D., Ai, Y."Hydrogen saline suppresses neuronal cell apoptosis and inhibits the p38 mitogen‑activated protein kinase‑caspase‑3 signaling pathway following cerebral ischemia‑reperfusion injury". Molecular Medicine Reports 16.4 (2017): 5321-5325.
Chicago
Li, D., Ai, Y."Hydrogen saline suppresses neuronal cell apoptosis and inhibits the p38 mitogen‑activated protein kinase‑caspase‑3 signaling pathway following cerebral ischemia‑reperfusion injury". Molecular Medicine Reports 16, no. 4 (2017): 5321-5325. https://doi.org/10.3892/mmr.2017.7294
Copy and paste a formatted citation
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Spandidos Publications style
Li D and Ai Y: Hydrogen saline suppresses neuronal cell apoptosis and inhibits the p38 mitogen‑activated protein kinase‑caspase‑3 signaling pathway following cerebral ischemia‑reperfusion injury. Mol Med Rep 16: 5321-5325, 2017.
APA
Li, D., & Ai, Y. (2017). Hydrogen saline suppresses neuronal cell apoptosis and inhibits the p38 mitogen‑activated protein kinase‑caspase‑3 signaling pathway following cerebral ischemia‑reperfusion injury. Molecular Medicine Reports, 16, 5321-5325. https://doi.org/10.3892/mmr.2017.7294
MLA
Li, D., Ai, Y."Hydrogen saline suppresses neuronal cell apoptosis and inhibits the p38 mitogen‑activated protein kinase‑caspase‑3 signaling pathway following cerebral ischemia‑reperfusion injury". Molecular Medicine Reports 16.4 (2017): 5321-5325.
Chicago
Li, D., Ai, Y."Hydrogen saline suppresses neuronal cell apoptosis and inhibits the p38 mitogen‑activated protein kinase‑caspase‑3 signaling pathway following cerebral ischemia‑reperfusion injury". Molecular Medicine Reports 16, no. 4 (2017): 5321-5325. https://doi.org/10.3892/mmr.2017.7294
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