Open Access

Oral administration of ampelopsin protects against acute brain injury in rats following focal cerebral ischemia

  • Authors:
    • Xiao‑Li Ye
    • Ling‑Qun Lu
    • Wei Li
    • Qi Lou
    • Hong‑Gang Guo
    • Qiao‑Juan Shi
  • View Affiliations

  • Published online on: March 8, 2017     https://doi.org/10.3892/etm.2017.4197
  • Pages: 1725-1734
  • Copyright: © Ye et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Ampelopsin (AMP) is isolated from the Chinese medicinal herb Ampelopsis grossedentata (Hand‑Mazz) and has been associated with numerous biological and pharmacological activities. However, it is not clear whether AMP has a direct protective effect on cerebral ischemia reperfusion injury. Therefore, the present study investigated its role in acute brain injury following focal cerebral ischemia in rats. The current study induced transient focal cerebral ischemia by performing middle cerebral artery occlusion (MCAO) for 60 min, followed by 24 h of reperfusion. Rats were exposed to 40, 80 and 160 mg/kg AMP by oral administration 30 min prior to MCAO and the cysteinyl leukotriene receptor 1‑antagonist, pranlukast (0.1 mg/kg, i.p.) was used as a positive control. Neurological deficit scores were observed and an inclined board test was used to assess behavioral dysfunction. The coronal slices were stained with 3,5‑triphenyltetrazolium chloride to determine the infarct volume and brain edema. Neuronal morphology was assessed in brain sections stained with cresyl violet and degenerating neurons were identified using Fluoro‑Jade B staining. Blood‑brain barrier permeability was determined with immunoglobulin (Ig)G immunohistochemistry. Interleukin (IL)‑1β, tumor necrosis factor‑α (TNF‑α) in serum and cerebrospinal fluid were measured using ELISA kits. AMP at 80 and 160 mg/kg attenuated neurological deficits, reduced infarct volume, brain edema, IgG exudation and neuron degeneration and loss. Similar to pranlukast, AMP also inhibited the MCAO‑induced IL‑1β and TNF‑α release. Thus, AMP has a neuroprotective effect on acute brain injury following focal cerebral ischemia in rats at an effective oral dose of 80‑160 mg/kg. The results of the current study indicate a therapeutic role for AMP in the treatment of ischemic stroke.
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May-2017
Volume 13 Issue 5

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

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Copy and paste a formatted citation
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Spandidos Publications style
Ye XL, Lu LQ, Li W, Lou Q, Guo HG and Shi QJ: Oral administration of ampelopsin protects against acute brain injury in rats following focal cerebral ischemia. Exp Ther Med 13: 1725-1734, 2017
APA
Ye, X., Lu, L., Li, W., Lou, Q., Guo, H., & Shi, Q. (2017). Oral administration of ampelopsin protects against acute brain injury in rats following focal cerebral ischemia. Experimental and Therapeutic Medicine, 13, 1725-1734. https://doi.org/10.3892/etm.2017.4197
MLA
Ye, X., Lu, L., Li, W., Lou, Q., Guo, H., Shi, Q."Oral administration of ampelopsin protects against acute brain injury in rats following focal cerebral ischemia". Experimental and Therapeutic Medicine 13.5 (2017): 1725-1734.
Chicago
Ye, X., Lu, L., Li, W., Lou, Q., Guo, H., Shi, Q."Oral administration of ampelopsin protects against acute brain injury in rats following focal cerebral ischemia". Experimental and Therapeutic Medicine 13, no. 5 (2017): 1725-1734. https://doi.org/10.3892/etm.2017.4197