Morin exerts neuroprotective actions in Parkinson disease models in vitro and in vivo
Abstract
Aim: To investigate the neuroprotective effects of morin on 1-methyl-4-phenylpyridinium ion (MPP+)-induced apoptosis in neuronal differentiated 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 μmol/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.
Keywords:
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 μmol/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.