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Article

Effect of hippocampal L‑NBP on BDNF and TrkB expression and neurological function of vascular dementia rats

  • Authors:
    • Yujing Huang
    • Zhaohui Li
    • Guangxian Nan
  • View Affiliations / Copyright

    Affiliations: Department of Neurology, China‑Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China, Department of Neurosurgery, China‑Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China
  • Pages: 7673-7678
    |
    Published online on: September 20, 2017
       https://doi.org/10.3892/mmr.2017.7539
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Abstract

The pathogenesis of vascular dementia (VD) is associated with neuronal degeneration, apoptosis or necrosis following ischemic brain injury. L‑butylphthalide (L‑NBP), has been demonstrated to exhibit potent anti‑ischemic and anti‑VD effects, however the associated specific mechanism remains to be elucidated. The present study generated a VD rat model, in which the effect of L‑NBP on neurological function and expression levels of brain‑derived neurotrophic factor (BDNF) and tyrosine kinase receptor B (TrkB) were observed. A total of 90 male Sprague Dawley rats were randomly divided into sham, model and L‑NBP groups (n=30). The VD model was generated by ligation of bilateral common carotid artery. A Morris water maze was used to test learning and memory functions. Animals were then sacrificed and cortical and hippocampal tissues were extracted. Hematoxylin and Eosin staining was used to observe brain tissue injury, and reverse transcription‑quantitative polymerase chain reaction was employed to measure BDNF and TrkB mRNA levels. Western blotting was employed to measure BDNF, TrkB and serine‑threonine protein kinase (Akt) protein levels. Immunohistochemistry staining was used to detect the N‑methyl‑D‑aspartate receptor (NMDAR) levels. VD rats exhibited elongated escape latency and lower crossing times, with significant neuronal damage. L‑NBP treatment shortened escape latency, increased crossing times and improved cortical and hippocampal injury. BDNF, TrkB, Akt and NMDAR expressions in the treatment group were significantly increased compared with the model group (P<0.05). L‑NBP may therefore enhance hippocampal expression of BDNF, TrkB, Akt and NMDAR, decrease ischemic injury of VD rats, and improve learning and memory.
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Copy and paste a formatted citation
Spandidos Publications style
Huang Y, Li Z and Nan G: Effect of hippocampal L‑NBP on BDNF and TrkB expression and neurological function of vascular dementia rats. Mol Med Rep 16: 7673-7678, 2017.
APA
Huang, Y., Li, Z., & Nan, G. (2017). Effect of hippocampal L‑NBP on BDNF and TrkB expression and neurological function of vascular dementia rats. Molecular Medicine Reports, 16, 7673-7678. https://doi.org/10.3892/mmr.2017.7539
MLA
Huang, Y., Li, Z., Nan, G."Effect of hippocampal L‑NBP on BDNF and TrkB expression and neurological function of vascular dementia rats". Molecular Medicine Reports 16.5 (2017): 7673-7678.
Chicago
Huang, Y., Li, Z., Nan, G."Effect of hippocampal L‑NBP on BDNF and TrkB expression and neurological function of vascular dementia rats". Molecular Medicine Reports 16, no. 5 (2017): 7673-7678. https://doi.org/10.3892/mmr.2017.7539
Copy and paste a formatted citation
x
Spandidos Publications style
Huang Y, Li Z and Nan G: Effect of hippocampal L‑NBP on BDNF and TrkB expression and neurological function of vascular dementia rats. Mol Med Rep 16: 7673-7678, 2017.
APA
Huang, Y., Li, Z., & Nan, G. (2017). Effect of hippocampal L‑NBP on BDNF and TrkB expression and neurological function of vascular dementia rats. Molecular Medicine Reports, 16, 7673-7678. https://doi.org/10.3892/mmr.2017.7539
MLA
Huang, Y., Li, Z., Nan, G."Effect of hippocampal L‑NBP on BDNF and TrkB expression and neurological function of vascular dementia rats". Molecular Medicine Reports 16.5 (2017): 7673-7678.
Chicago
Huang, Y., Li, Z., Nan, G."Effect of hippocampal L‑NBP on BDNF and TrkB expression and neurological function of vascular dementia rats". Molecular Medicine Reports 16, no. 5 (2017): 7673-7678. https://doi.org/10.3892/mmr.2017.7539
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