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Cyanidin suppresses amyloid beta-induced neurotoxicity by inhibiting reactive oxygen speciesmediated DNA damage and apoptosis in PC12 cells 被引量:3
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作者 Yi Wang xiao-ting fu +7 位作者 Da-wei Li Kun Wang Xin-zhi Wang Yuan Li Bao-liang Sun Xiao-yi Yang Zun-cheng Zheng Nam Chun Cho 《Neural Regeneration Research》 SCIE CAS CSCD 2016年第5期795-800,共6页
Amyloid beta(Aβ)-induced oxidative stress is a major pathologic hallmark of Alzheimer's disease. Cyanidin, a natural flavonoid compound, is neuroprotective against oxidative damage-mediated degeneration. However, ... Amyloid beta(Aβ)-induced oxidative stress is a major pathologic hallmark of Alzheimer's disease. Cyanidin, a natural flavonoid compound, is neuroprotective against oxidative damage-mediated degeneration. However, its molecular mechanism remains unclear. Here, we investigated the effects of cyanidin pretreatment against Aβ-induced neurotoxicity in PC12 cells, and explored the underlying mechanisms. Cyanidin pretreatment significantly attenuated Aβ-induced cell mortality and morphological changes in PC12 cells. Mechanistically, cyanidin effectively blocked apoptosis induced by Aβ, by restoring the mitochondrial membrane potential via upregulation of Bcl-2 protein expression. Moreover, cyanidin markedly protected PC12 cells from Aβ-induced DNA damage by blocking reactive oxide species and superoxide accumulation. These results provide evidence that cyanidin suppresses Aβ-induced cytotoxicity, by preventing oxidative damage mediated by reactive oxide species, which in turn inhibits mitochondrial apoptosis. Our study demonstrates the therapeutic potential of cyanidin in the prevention of oxidative stress-mediated Aβ neurotoxicity. 展开更多
关键词 nerve regeneration CYANIDIN AMYLOID-BETA oxidative damage reactive oxide species APOPTOSIS neural regeneration
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Selenocysteine antagonizes oxygen glucose deprivation-induced damage to hippocampal neurons 被引量:2
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作者 Xian-Jun Wang Mei-Hong Wang +5 位作者 xiao-ting fu Ya-Jun Hou Wang Chen Da-Chen Tian Su-Yun Bai Xiao-Yan fu 《Neural Regeneration Research》 SCIE CAS CSCD 2018年第8期1433-1439,共7页
Designing and/or searching for novel antioxidants against oxygen glucose effective strategy for the treatment of human isdlemic stroke. Selenium is deprivation (OGD)-induced oxidative damage represents an an essenti... Designing and/or searching for novel antioxidants against oxygen glucose effective strategy for the treatment of human isdlemic stroke. Selenium is deprivation (OGD)-induced oxidative damage represents an an essential trace dement, which is beneficial in the chemo- prevention and chemotherapy of cerebral ischemic stroke. The underlying mechanisms for its therapeutic effects, however, are not well documented. Selenocysteine (SeC) is a selenium-containing amino acid with neuroprotective potential. Studies have shown that SeC can reduce irradiation-induced DNA apoptosis by reducing DNA damage. In this study, the in vitro protective potential and mechanism of action of SeC against OGD-induced apoptosis and neurotoxicity were evaluated in HT22 mouse hippocampal neurons. We cultured HT22 cells in a glucose-free medium containing 2 mM Na2S402, which formed an OGD environment, for 90 minutes. Findings from MTT, flow cytometry and TUNEL staining showed obvious cytotoxicity and apoptosis in HT22 cells in the OGD condition. The activation of Caspa se-7 and Caspase-9 further revealed that OGD-induced apoptosis of HT22 cells was mainly achieved by triggering a mitochondrial-medi- ated pathway. Moreover, the OGD condition also induced serious DNA damage through the accumulation of reactive oxygen species and superoxide anions. However, SeC pre-treatment for 6 hours effectively inhibited OGD-induced cytotoxicity and apoptosis in HT22 cells by inhibiting reactive oxygen species-mediated oxidative damage. Our findings provide evidence that SeC has the potential to suppress OGD-induced oxidative damage and apoptosis in hippocampal neurons. 展开更多
关键词 SELENIUM SELENOCYSTEINE ischemic stroke oxygen glucose deprivation hippocampal neuron MITOCHONDRIA reaction oxygen species superoxide anion oxidative damage APOPTOSIS
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An algorithm for preferential selection of spectroscopic targets in LEGUE 被引量:1
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作者 Jeffrey L. Carlin Sebastien Lepine +22 位作者 Heidi Jo Newberg Li-Cai Deng Timothy C. Beers Yu-Qin Chen Norbert Christlie xiao-ting fu Shuang Gao Carl J. Grillmair PuragraGuhathakurta Zhan-Wen Han Jin-Liang Hou Hsu-Tai Lee Jing Li Chao Liu Xiao-Wei Liu Kai-Ke Pan J. A. Sellwood Hong-Chi Wang Fan Yang Brian Yanny Yue-Yang Zhan Zheng Zheng Zi Zhu 《Research in Astronomy and Astrophysics》 SCIE CAS CSCD 2012年第7期755-771,共17页
We describe a general target selection algorithm that is applicable to any survey in which the number of available candidates is much larger than the number of objects to be observed. This routine aims to achieve a ba... We describe a general target selection algorithm that is applicable to any survey in which the number of available candidates is much larger than the number of objects to be observed. This routine aims to achieve a balance between a smoothly- varying, well-understood selection function and the desire to preferentially select cer- tain types of targets. Some target-selection examples are shown that illustrate differentpossibilities of emphasis functions. Although it is generally applicable, the algorithm was developed specifically for the LAMOST Experiment for Galactic Understanding and Exploration (LEGUE) survey that will be carried out using the Chinese Guo Shou Jing Telescope. In particular, this algorithm was designed for the portion of LEGUE targeting the Galactic halo, in which we attempt to balance a variety of science goals that require stars at fainter magnitudes than can be completely sampled by LAMOST. This algorithm has been implemented for the halo portion of the LAMOST pilot sur- vey, which began in October 2011. 展开更多
关键词 surveys: LAMOST -- Galaxy: halo -- techniques: spectroscopic
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