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首页> 外文期刊>Journal of Ginseng Research >Ginsenoside Rb2 suppresses the glutamate-mediated oxidative stress and neuronal cell death in HT22 cells
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Ginsenoside Rb2 suppresses the glutamate-mediated oxidative stress and neuronal cell death in HT22 cells

机译：人参皂苷Rb2抑制谷氨酸介导的HT22细胞中的氧化应激和神经元细胞死亡

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Background The objective of our study was to analyze the neuroprotective effects of ginsenoside derivatives Rb1, Rb2, Rc, Rd, Rg1, and Rg3 against glutamate-mediated neurotoxicity in HT22 hippocampal mouse neuron cells. Methods The neuroprotective effect of ginsenosides were evaluated by measuring cell viability. Protein expressions of mitogen-activated protein kinase (MAPK), Bcl2, Bax, and apoptosis-inducing factor (AIF) were determined by Western blot analysis. The occurrence of apoptotic and death cells was determined by flow cytometry. Cellular level of Casup2+/sup and reactive oxygen species (ROS) levels were evaluated by image analysis using the fluorescent probes Fluor-3 and 2′,7′-dichlorodihydrofluorescein diacetate, respectively. In?vivo efficacy of neuroprotection was evaluated using the Mongolian gerbil of ischemic brain injury model. Result Reduction of cell viability by glutamate (5 mM) was significantly suppressed by treatment with ginsenoside Rb2. Phosphorylation of MAPKs, Bax, and nuclear AIF was gradually increased by treatment with 5 mM of glutamate and decreased by co-treatment with Rb2. The occurrence of apoptotic cells was decreased by treatment with Rb2 (25.7 μM). Cellular Casup2+/sup and ROS levels were decreased in the presence of Rb2, and in?vivo data indicated that Rb2 treatment (10 mg/kg) significantly diminished the number of degenerated neurons. Conclusion Our results suggest that Rb2 possesses neuroprotective properties that suppress glutamate-induced neurotoxicity. The molecular mechanism of Rb2 is by suppressing the MAPKs activity and AIF translocation.
机译：背景技术我们的研究目的是分析人参皂甙衍生物Rb1，Rb2，Rc，Rd，Rg1和Rg3对谷氨酸介导的HT22海马小鼠神经元细胞的神经保护作用。方法通过测定细胞活力评价人参皂苷的神经保护作用。通过蛋白质印迹分析确定了促分裂原活化蛋白激酶（MAPK），Bcl2，Bax和凋亡诱导因子（AIF）的蛋白表达。通过流式细胞术确定凋亡和死亡细胞的发生。分别使用荧光探针Fluor-3和2'，7'-dichlorodihydrofluorescein diacetate荧光探针通过图像分析来评估细胞内Ca 2 + 和活性氧（ROS）的水平。使用蒙古沙鼠缺血性脑损伤模型评估了神经保护作用的体内有效性。结果人参皂甙Rb2处理可明显抑制谷氨酸（5 mM）降低的细胞活力。 MAPK，Bax和核AIF的磷酸化通过5 mM谷氨酸处理逐渐增加，而与Rb2共同处理则降低。用Rb2（25.7μM）处理可减少凋亡细胞的发生。在存在Rb2的情况下，细胞Ca 2 + 和ROS的水平降低，体内数据表明，Rb2处理（10 mg / kg）显着减少了变性神经元的数量。结论我们的结果表明Rb2具有抑制谷氨酸诱导的神经毒性的神经保护特性。 Rb2的分子机制是通过抑制MAPKs活性和AIF易位。

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