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酸枣仁通过抗氧化作用减轻沙土鼠海马区的缺血性损伤。

Zizyphus attenuates ischemic damage in the gerbil hippocampus via its antioxidant effect.

机构信息

Department of Anatomy and Neurobiology, Institute of Neurodegeneration and Neuroregeneration, College of Medicine, Hallym University, Chuncheon, Republic of Korea.

出版信息

J Med Food. 2010 Jun;13(3):557-63. doi: 10.1089/jmf.2009.1254.

Abstract

The fruit of Zizyphus jujuba has been used as a traditional Chinese medicinal herb and considered for thousands of years to affect various physiological functions in the body. We obtained a Z. jujuba extract (ZJE) and observed the neuroprotective effects of ZJE against ischemic damage in gerbils that had received repeated oral administrations of ZJE for 10 days. In the ZJE-treated ischemia group, neuronal nuclei (a marker for neurons)-immunoreactive neurons were abundant (58.4% vs. sham group) in the hippocampal CA1 region 4 days after ischemia/reperfusion compared to those in the vehicle-treated ischemia group (11.3%). In addition, ZJE treatment significantly decreased the reactive gliosis of astrocytes and microglia in the CA1 region compared to that in the vehicle-treated group 4 days after ischemia/reperfusion. Immunoreactivities of Cu,Zn-superoxide dismutase (SOD1) and brain-derived neurotrophic factor in the ZJE-treated ischemia group were higher those in the vehicle-treated ischemia group 4 days after ischemia/reperfusion. In addition, in the ZJE-treated ischemia group, levels of hydroxynonenal, an indicator of lipid peroxidation, were much lower than those in the vehicle-treated ischemia group after ischemia/reperfusion. These results suggest that the repeated supplements of ZJE can protect neurons from ischemic damage via up-regulation of SOD1 and reduction of lipid peroxidation in the ischemic hippocampal CA1 region.

摘要

酸枣仁的果实被用作传统中药,几千年来被认为对人体的各种生理功能有影响。我们获得了酸枣仁提取物(ZJE),并观察了 ZJE 对接受重复口服 ZJE 治疗 10 天的沙土鼠缺血损伤的神经保护作用。在 ZJE 治疗的缺血组中,与 Vehicle 治疗的缺血组相比,缺血再灌注后 4 天海马 CA1 区神经元核(神经元标志物)免疫反应性神经元丰富(58.4% vs. sham 组)。此外,与 Vehicle 治疗的缺血组相比,ZJE 治疗在缺血再灌注后 4 天显著降低了 CA1 区星形胶质细胞和小胶质细胞的反应性胶质增生。缺血再灌注后 4 天,ZJE 治疗的缺血组中 Cu,Zn-超氧化物歧化酶(SOD1)和脑源性神经营养因子的免疫反应性高于 Vehicle 治疗的缺血组。此外,在 ZJE 治疗的缺血组中,缺血再灌注后羟自由基(脂质过氧化的指标)的水平明显低于 Vehicle 治疗的缺血组。这些结果表明,重复补充 ZJE 可以通过上调 SOD1 和减少缺血海马 CA1 区的脂质过氧化来保护神经元免受缺血损伤。

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