Xu Ai-Ling, Zheng Guan-Yi, Wang Zhi-Jian, Chen Xiao-Dong, Jiang Qiong
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.
Mol Med Rep. 2016 Apr;13(4):2957-66. doi: 10.3892/mmr.2016.4921. Epub 2016 Feb 22.
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.
冬凌草甲素是从一种常用于传统中药的植物根部分离出的化合物。本研究的目的是探讨冬凌草甲素对大脑中动脉闭塞(MCAO)大鼠的可能保护机制。通过2小时的MCAO诱导短暂性局灶性脑缺血,随后进行再灌注。在缺血/再灌注后立即通过腹腔注射给予剂量为20、40和80mg/kg的冬凌草甲素。使用免疫染色和Western印迹分析对缺血/再灌注后梗死周围区域的胶质纤维酸性蛋白(GFAP)、离子钙结合衔接分子1(Iba-1)、血管内皮生长因子(VEGF)、胎儿肝激酶-1(Flk-1)和巢蛋白的表达水平进行检测。冬凌草甲素以剂量依赖性方式显著降低梗死体积并改善神经功能缺损。与给予生理盐水的大鼠相比,用冬凌草甲素治疗的大鼠中VEGF、Flk-1和巢蛋白的表达水平显著升高。在用冬凌草甲素治疗后,与仅暴露于缺血的大鼠相比,在第1、3和7天,在接受冬凌草甲素治疗的大鼠中发现更多GFAP阳性星形胶质细胞,然而,与缺血组相比,在第14天星形胶质细胞较少。冬凌草甲素显著降低Iba-1的蛋白表达。本研究结果表明,冬凌草甲素的保护作用与血管再生、神经元再生以及星形胶质细胞和小胶质细胞活化的调节有关。