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作 者:Ling Qu Xiaochun Liang Bei Gu Wei Liu
机构地区:[1]Department of Traditional Chinese Medicine, Peking Union Medical College Hospital, Peking Union Medical College, China Academy of Medical Sciences [2]Cell Center, Institute of Basic Medical Science, Peking Union Medical College, China Academy of Medical Sciences
出 处:《Neural Regeneration Research》2014年第12期1195-1203,共9页中国神经再生研究(英文版)
基 金:supported by the National Natural Science Foundation of China,No.30572438;the Beijing Science Nuture Foundation,No.7132189;a grant from Science Foundation of Peking Union Medical College Hospital,No.2013-098
摘 要:Quercetin can reverse high glucose-induced inhibition of neural cell proliferation, and therefore may have a neuroprotective effect in diabetic peripheral neuropathy. It is difficult to obtain pri- mary Schwann cells and RSC96 cells could replace primary Schwann cells in studies of the role of autophagy in the mechanism underlying diabetic peripheral neuropathy. Here, we show that under high glucose conditions, there are fewer autophagosomes in immortalized rat RSC96 cells and primary rat Schwann ceils than under control conditions, the proliferative activity of both cell types is significantly impaired, and the expression of Berlin- 1 and LC3, the molecular mark- ers for autophagy, is significantly lower. After intervention with quercetin, the autophagic and proliferative activity of both cell types is rescued. These results suggest that quercetin can allevi- ate high glucose-induced damage to Schwann cells by autophagy.Quercetin can reverse high glucose-induced inhibition of neural cell proliferation, and therefore may have a neuroprotective effect in diabetic peripheral neuropathy. It is difficult to obtain pri- mary Schwann cells and RSC96 cells could replace primary Schwann cells in studies of the role of autophagy in the mechanism underlying diabetic peripheral neuropathy. Here, we show that under high glucose conditions, there are fewer autophagosomes in immortalized rat RSC96 cells and primary rat Schwann ceils than under control conditions, the proliferative activity of both cell types is significantly impaired, and the expression of Berlin- 1 and LC3, the molecular mark- ers for autophagy, is significantly lower. After intervention with quercetin, the autophagic and proliferative activity of both cell types is rescued. These results suggest that quercetin can allevi- ate high glucose-induced damage to Schwann cells by autophagy.
关 键 词:nerve regeneration QUERCETIN diabetic peripheral neuropathy high glucose RSC96 primary Schwann cells proliferation ULTRASTRUCTURE AUTOPHAGY BECLIN-1 LC3 NSFC grant neural regeneration
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