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Neuroprotective effects of Ilexonin A following transient focal cerebral ischemia in rats

  • Authors:
    • Ai‑Ling Xu
    • Guan‑Yi Zheng
    • Zhi‑Jian Wang
    • Xiao‑Dong Chen
    • Qiong Jiang
  • View Affiliations / Copyright

    Affiliations: Department of Traditional Chinese Medicine, The Affiliated Union Hospital of Fujian Medical University, Fuzhou, Fujian 350001, P.R. China, Burns Institute of the Affliated Union Hospital of Fujian Medical University, Fuzhou, Fujian 350001, P.R. China
    Copyright: © Xu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 2957-2966
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    Published online on: February 22, 2016
       https://doi.org/10.3892/mmr.2016.4921
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Abstract

Ilexonin A is a compound isolated from the root of a plant commonly used in traditional Chinese medicine. The aim of the present study was to investigate the possible protective mechanism of Ilexonin A in rats subjected to occlusion of the middle cerebral artery (MCAO). Transient focal cerebral ischemia was induced by 2 h of MCAO, followed by reperfusion. Ilexonin A at doses of 20, 40 and 80 mg/kg were administered via intraperitoneal injection immediately following ischemia/reperfusion. The expression levels of glial fibrillary acidic protein (GFAP), ionized calcium‑binding adapter molecule‑1 (Iba‑1), vascular endothelial growth factor (VEGF), fetal liver kinase‑1 (Flk‑1) and Nestin were examined using immunostaining and Western blot analysis of the peri‑infarct region following ischemia/reperfusion. Ilexonin A significantly decreased the infarct volume and improved neurological deficits in a dose‑dependent manner. The expression levels of VEGF, Flk‑1 and Nestin were significantly increased in the rats treated with Ilexonin A, compared with the rats administered with saline. Following treatment with Ilexonin A, a higher number of GFAP‑positive astrocytes were found in the Ilexonin A‑treated rats at 1, 3 and 7 days, compared with the rats exposed to ischemia only, however, there were fewer astrocytes at 14 days, compared with the ischemia group. Ilexonin A significantly decreased the protein expression of Iba‑1. The results of the present study suggested that the protective effects of Ilexonin A were associated with revascularization, neuronal regeneration, and the regulation of astrocyte and microglia cell activation.
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Spandidos Publications style
Xu AL, Zheng GY, Wang ZJ, Chen XD and Jiang Q: Neuroprotective effects of Ilexonin A following transient focal cerebral ischemia in rats. Mol Med Rep 13: 2957-2966, 2016.
APA
Xu, A., Zheng, G., Wang, Z., Chen, X., & Jiang, Q. (2016). Neuroprotective effects of Ilexonin A following transient focal cerebral ischemia in rats. Molecular Medicine Reports, 13, 2957-2966. https://doi.org/10.3892/mmr.2016.4921
MLA
Xu, A., Zheng, G., Wang, Z., Chen, X., Jiang, Q."Neuroprotective effects of Ilexonin A following transient focal cerebral ischemia in rats". Molecular Medicine Reports 13.4 (2016): 2957-2966.
Chicago
Xu, A., Zheng, G., Wang, Z., Chen, X., Jiang, Q."Neuroprotective effects of Ilexonin A following transient focal cerebral ischemia in rats". Molecular Medicine Reports 13, no. 4 (2016): 2957-2966. https://doi.org/10.3892/mmr.2016.4921
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Spandidos Publications style
Xu AL, Zheng GY, Wang ZJ, Chen XD and Jiang Q: Neuroprotective effects of Ilexonin A following transient focal cerebral ischemia in rats. Mol Med Rep 13: 2957-2966, 2016.
APA
Xu, A., Zheng, G., Wang, Z., Chen, X., & Jiang, Q. (2016). Neuroprotective effects of Ilexonin A following transient focal cerebral ischemia in rats. Molecular Medicine Reports, 13, 2957-2966. https://doi.org/10.3892/mmr.2016.4921
MLA
Xu, A., Zheng, G., Wang, Z., Chen, X., Jiang, Q."Neuroprotective effects of Ilexonin A following transient focal cerebral ischemia in rats". Molecular Medicine Reports 13.4 (2016): 2957-2966.
Chicago
Xu, A., Zheng, G., Wang, Z., Chen, X., Jiang, Q."Neuroprotective effects of Ilexonin A following transient focal cerebral ischemia in rats". Molecular Medicine Reports 13, no. 4 (2016): 2957-2966. https://doi.org/10.3892/mmr.2016.4921
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