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Hydroxybutyrate promotes the recovery from cerebral infarction by activating Amp‑activated protein kinase signaling

  • Authors:
    • Huisheng Wu
    • Peipei Guo
    • Xinyi Li
    • Zhao Jin
    • Xin Yang
    • Yanlin Wang
  • View Affiliations / Copyright

    Affiliations: Department of Anesthesiology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei 430071, P.R. China
    Copyright: © Wu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1195-1202
    |
    Published online on: June 13, 2018
       https://doi.org/10.3892/etm.2018.6304
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Abstract

Recent studies have shown that hydroxybutyrate (GHB) is effective for protection against ischemia/brain damage in rat models. However, the specific underlying mechanism is poorly understood. In line with the previous studies, the present data showed that GHB improves cerebral blood flow (CBF) and physiological variables, including pH, pCO2 and pO2. Using CD31‑immunofluorescence staining, a reduction of blood vessel density was indicated in the middle cerebral artery occlusion (MCAO) group; however, GHB treatment enhanced the cerebral vascular density in the ischemic area. In addition, GHB treatment increased the number of BrdU/lectin double‑positive cells. Furthermore, the reduction of nestin‑positive cells was identified in the brain of MCAO rats, while the number of nestin‑positive cells was significantly increased after GHB administration. Compared with the sham group, the activation of Amp‑activated protein kinase (AMPK) was identified in MCAO rats, suggesting stress‑mediated AMPK activation after ischemia. Furthermore, the western blot assay showed that GHB treatment resulted in further activation of AMPK and endothelial nitric oxide synthase (eNOS), suggesting an enhanced energy supply. In summary, the present novel data indicates that GHB promotes the recovery from cerebral infarction mainly by activating AMPK and eNOS signaling, thereby enhancing angiogenesis and neuron regeneration.
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Copy and paste a formatted citation
Spandidos Publications style
Wu H, Guo P, Li X, Jin Z, Yang X and Wang Y: Hydroxybutyrate promotes the recovery from cerebral infarction by activating Amp‑activated protein kinase signaling. Exp Ther Med 16: 1195-1202, 2018.
APA
Wu, H., Guo, P., Li, X., Jin, Z., Yang, X., & Wang, Y. (2018). Hydroxybutyrate promotes the recovery from cerebral infarction by activating Amp‑activated protein kinase signaling. Experimental and Therapeutic Medicine, 16, 1195-1202. https://doi.org/10.3892/etm.2018.6304
MLA
Wu, H., Guo, P., Li, X., Jin, Z., Yang, X., Wang, Y."Hydroxybutyrate promotes the recovery from cerebral infarction by activating Amp‑activated protein kinase signaling". Experimental and Therapeutic Medicine 16.2 (2018): 1195-1202.
Chicago
Wu, H., Guo, P., Li, X., Jin, Z., Yang, X., Wang, Y."Hydroxybutyrate promotes the recovery from cerebral infarction by activating Amp‑activated protein kinase signaling". Experimental and Therapeutic Medicine 16, no. 2 (2018): 1195-1202. https://doi.org/10.3892/etm.2018.6304
Copy and paste a formatted citation
x
Spandidos Publications style
Wu H, Guo P, Li X, Jin Z, Yang X and Wang Y: Hydroxybutyrate promotes the recovery from cerebral infarction by activating Amp‑activated protein kinase signaling. Exp Ther Med 16: 1195-1202, 2018.
APA
Wu, H., Guo, P., Li, X., Jin, Z., Yang, X., & Wang, Y. (2018). Hydroxybutyrate promotes the recovery from cerebral infarction by activating Amp‑activated protein kinase signaling. Experimental and Therapeutic Medicine, 16, 1195-1202. https://doi.org/10.3892/etm.2018.6304
MLA
Wu, H., Guo, P., Li, X., Jin, Z., Yang, X., Wang, Y."Hydroxybutyrate promotes the recovery from cerebral infarction by activating Amp‑activated protein kinase signaling". Experimental and Therapeutic Medicine 16.2 (2018): 1195-1202.
Chicago
Wu, H., Guo, P., Li, X., Jin, Z., Yang, X., Wang, Y."Hydroxybutyrate promotes the recovery from cerebral infarction by activating Amp‑activated protein kinase signaling". Experimental and Therapeutic Medicine 16, no. 2 (2018): 1195-1202. https://doi.org/10.3892/etm.2018.6304
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