Protective effects of notoginsenoside R1 on cerebral ischemia-reperfusion injury in rats.
Protective effects of notoginsenoside R1 on cerebral ischemia-reperfusion injury in rats.
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DOI：
10.3892/etm.2017.5268
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发表时间：
2017-12
影响因子：
2.7
通讯作者：
Ban L
中科院分区：
文献类型：
--
作者：
Zou S;Zhang M;Feng L;Zhou Y;Li L;Ban L
本研究旨在探讨神经生长因子受体1（NGR 1）对大鼠脑缺血再灌注损伤（CIRI）的保护作用及其分子机制，为CIRI的诊断和治疗提供新的思路。将60只SD大鼠随机分为假手术组（Sham）、脑缺血再灌注模型组（CIR）、NGR 1治疗组（NGR 1）和尼莫地平阳性对照组（NDC），每组15只。采用双侧颈总动脉夹闭法建立大鼠CIRI模型。采用氯化三苯基四氮唑染色法计算再灌注结束时脑梗死面积。Annexin V/碘化丙啶双染法检测各组海马神经元凋亡情况。采用RT-qPCR和western blot方法分别检测再灌注结束时海马脑源性神经营养因子（brain-derived neurotrophic factor，BDNF）mRNA、Bcl-2和Bax蛋白表达。采用SPSS软件进行统计分析，确保统计学意义。再灌注结束时，NGR 1和NDC组的脑梗死面积明显小于CIR组。细胞凋亡分析显示，与CIR组相比，NGR 1和NDC组海马神经元凋亡率明显降低。RT-qPCR和western blot分析显示，再灌注结束时，NGR 1和NDC组海马中BDNF mRNA和抗凋亡因子Bcl-2的水平高于CIR组，而促凋亡因子Bax的水平低于CIR组。NGR 1对CIRI的保护作用明显强于尼莫地平。结论：NGR 1可缩小脑梗死面积，减少海马神经元凋亡，对CIRI大鼠具有保护作用。这些作用是通过激活BDNF和Bcl-2的表达以及抑制Bax的表达来实现的。
The objective of this study was to investigate the protective effect of notoginsenoside R1 (NGR1) on cerebral ischemia-reperfusion injury (CIRI) in rats, and its molecular mechanism, to provide new insights into the diagnosis and treatment of CIRI. Sixty Sprague-Dawley rats were randomly divided into four groups including the sham-operation group (Sham), cerebral ischemia-reperfusion model group (CIR), NGR1 treatment group (NGR1), and nimodipine positive control group (NDC) with 15 rats each. Bilateral common carotid arteries occlusion was used to establish the rat CIRI model. The area of cerebral infarction at the end of reperfusion was calculated by triphenyl tetrazolium chloride staining. Apoptosis of hippocampal neurons in each group was detected by Annexin V/propidium iodide double staining. Hippocampal expression of brain-derived neurotrophic factor (BDNF) mRNA, and Bcl-2 and Bax protein at the end of reperfusion were measured by RT-qPCR and western blot analysis, respectively. Data were analyzed by SPSS software analysis to ensure statistical significance. At the end of reperfusion, the area of cerebral infarction in the NGR1 and NDC groups was significantly smaller than that of the CIR group. Apoptosis analysis showed that compared with the CIR group, the apoptosis rate of hippocampal neurons was significantly decreased in the NGR1 and NDC groups. RT-qPCR and western blot analysis showed that at the end of reperfusion, higher levels of BDNF mRNA and the anti-apoptotic factor, Bcl-2, and lower levels of the pro-apoptotic factor, Bax, in the hippocampus were found in the NGR1 and NDC groups compared with the CIR group. The protective effect of NGR1 on CIRI was significantly stronger than that of nimodipine. In conclusion, NGR1 can reduce the area of cerebral infarction, reduce apoptosis of hippocampal neurons, and protect rats from CIRI. Those effects were achieved by activating the expression of BDNF and Bcl-2, and by inhibiting the expression of Bax.
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