Morin exerts neuroprotective actions in Parkinson disease models in vitro and in vivo  

作　　者：Zhen-tao ZHANG Xue-bing CAO Nian XlONG Hong-cai WANG Jin-sha HUANG Sheng-gang SUN Tao WANG 

机构地区：[1]Department of Neurology, Renmin Hospital of Wuhan University, Wuhan 430060, China [2]Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China

出　　处：《Acta Pharmacologica Sinica》2010年第8期900-906,共7页中国药理学报（英文版）

基　　金：Acknowledgements This work was supported by grants from National Natural Science Foundation of China （No 30570627 and No 30870866）.

摘　　要：Aim： To investigate the neuroprotective effects of morin on 1-methyt-4-phenylpyridinium ion （MPP＋）-induced apoptosis in neuronal dif- ferentiated PC12 cells as well as in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine （MPTP） mouse model of Parkinson disease （PD）. Methods： PC12 cells were challenged with MPP in the presence or absence of morin. Cell viability was determined using MTT assay. Cell apoptosis was measured using flow cytometry. Generation of reactive oxygen species （ROS） was assayed using fluorescence assay. In an MPTP mouse model of PD, behavioral deficits, striatal dopamine content, and number of dopaminergic neurons were measured. Results： MPP~ induced apoptosis and ROS formation in PC12 cells. Concomitant treatment with morin （5-50 IJmol/L） significantly attenuated the loss of cell viability and apoptosis when compared with MPP~ treatment alone. Morin also attenuated ROS formation induced by MPP . MPTP induced permanent behavioral deficits and nigrostriatal lesions in mice. When administered prior to MPTP, morin （20 to 100 mg/kg） attenuated behavioral deficits, dopaminergic neuronal death and striatal dopamine depletion in the MPTP mouse model. Conclusion： The findings suggest that morin has neuroprotective actions both in vitro and in vivo, and may provide a novel therapeutic agent for the treatment of PD and other neurodegenerative diseases.Aim： To investigate the neuroprotective effects of morin on 1-methyt-4-phenylpyridinium ion （MPP＋）-induced apoptosis in neuronal dif- ferentiated PC12 cells as well as in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine （MPTP） mouse model of Parkinson disease （PD）. Methods： PC12 cells were challenged with MPP in the presence or absence of morin. Cell viability was determined using MTT assay. Cell apoptosis was measured using flow cytometry. Generation of reactive oxygen species （ROS） was assayed using fluorescence assay. In an MPTP mouse model of PD, behavioral deficits, striatal dopamine content, and number of dopaminergic neurons were measured. Results： MPP~ induced apoptosis and ROS formation in PC12 cells. Concomitant treatment with morin （5-50 IJmol/L） significantly attenuated the loss of cell viability and apoptosis when compared with MPP~ treatment alone. Morin also attenuated ROS formation induced by MPP . MPTP induced permanent behavioral deficits and nigrostriatal lesions in mice. When administered prior to MPTP, morin （20 to 100 mg/kg） attenuated behavioral deficits, dopaminergic neuronal death and striatal dopamine depletion in the MPTP mouse model. Conclusion： The findings suggest that morin has neuroprotective actions both in vitro and in vivo, and may provide a novel therapeutic agent for the treatment of PD and other neurodegenerative diseases.

关 键 词：MORIN apoptosis PC12 cells MPTP Parkinson disease DOPAMINE 

分 类 号：Q257[生物学—细胞生物学] TS218[轻工技术与工程—粮食、油脂及植物蛋白工程]