Neurotrophic effects of 7,8-dihydroxycoumarin in primary cultured rat cortical neurons  

作　　者：Li Yan Xiaowen Zhou Xing Zhou Zheng Zhang Huan-Min Luo 

机构地区：[1]Department of Pharmacology, School of Medicine [2]Institute of Brain Sciences, Jinan University, Guangzhou 510632, China [3]The Joint Laboratory of Brain Function and Health, Jinan University and The University of Hong Kong, Jinan University, Guangzhou 510632, China

出　　处：《Neuroscience Bulletin》2012年第5期493-498,共6页神经科学通报（英文版）

基　　金：supported by grants from the National Natural Science Foundation of China (30672450);the National Basic Research Development Program (973 Program) of China (2011CB707500);the Third Stage Construction Funds of National "Project 211", Department of Education, China (2005–2010)

摘　　要：Objective Neuronal loss in the central nervous system is central to the occurrence of neurodegenerative diseases. Pharmaceutical companies have devoted much effort to developing new drugs against such diseases, since there are currently no effective drugs for neurodegenerative disease treatment. Promoting the capacity for nerve regeneration is an ideal treatment target. The present study aimed to investigate the neurotrophic effects of 7,8-dihydroxycoumarin （DHC） or daphnetin in primary cultured rat cortical neurons. Methods Cortical neurons were identified by microtubule-associated protein 2 （MAP2） immunostaining. Morphological observation was used to measure the average length of neurite outgrowth. MTT and lactate dehydrogenase assays were used to assess neuronal survival. The mRNA expression of MAP2 and brain-derived neurotrophic factor （BDNF） was measured by RT-PCR. Results MAP2 immunostaining showed that most of the cultured cells were neurons. Compared with the vehicle control group, DHC promoted neurite outgrowth and prolonged neuronal survival time at concentrations ranging from 2 to 8 μmol/L. Expression of both BDNF mRNA and MAP2 mRNAwas increased in the groups treated with 2, 4 and 8 μmol/L DHC. Conclusion DHC significantly increases neurite outgrowth and promotes neuronal survival in primary cultured rat cortical neurons. The neurotrophic effects of DHC are probably associated with increased BDNF expression.Objective Neuronal loss in the central nervous system is central to the occurrence of neurodegenerative diseases. Pharmaceutical companies have devoted much effort to developing new drugs against such diseases, since there are currently no effective drugs for neurodegenerative disease treatment. Promoting the capacity for nerve regeneration is an ideal treatment target. The present study aimed to investigate the neurotrophic effects of 7,8-dihydroxycoumarin （DHC） or daphnetin in primary cultured rat cortical neurons. Methods Cortical neurons were identified by microtubule-associated protein 2 （MAP2） immunostaining. Morphological observation was used to measure the average length of neurite outgrowth. MTT and lactate dehydrogenase assays were used to assess neuronal survival. The mRNA expression of MAP2 and brain-derived neurotrophic factor （BDNF） was measured by RT-PCR. Results MAP2 immunostaining showed that most of the cultured cells were neurons. Compared with the vehicle control group, DHC promoted neurite outgrowth and prolonged neuronal survival time at concentrations ranging from 2 to 8 μmol/L. Expression of both BDNF mRNA and MAP2 mRNAwas increased in the groups treated with 2, 4 and 8 μmol/L DHC. Conclusion DHC significantly increases neurite outgrowth and promotes neuronal survival in primary cultured rat cortical neurons. The neurotrophic effects of DHC are probably associated with increased BDNF expression.

关 键 词：7 8-dihydroxycoumarin DAPHNETIN rat cortical neurons brain-derived neurotrophic factor neurodegenerative disease 

分 类 号：Q424[生物学—神经生物学] S831.1[生物学—生理学]