Abstract: ［Abstract］  Objective〖HTSS〗〓To investigate the effects and mechanisms of Baicalein on autophage activation and the removal of abnormal alphasynuclein aggragation in Parkinson disease. And to observe the protective effect of baicalein on mitochondrial damage induced by alphasynuclein.
〖HTH〗〖WTHZ〗Methods〖HTSS〗〓The overexpression of alphasynuclein model was established in PC12 cells. Then the cells were treated by different concentrations of Baicalein. The degradation of alphasynuclein was detected by confocal laser scanning microscopy. Finally, the cell lactate dehydrogenase release was examined by use of LDH kit.
〖HTH〗〖WTHZ〗Results〖HTSS〗〓Baicalein can dosedependently reduce the expression level of alphasynuclein, activate autophagy markers LC3 and decrease the level of autophagy substrate p62. Immunofluorescence and western blotting show that Baicalein can inhibit mamamalian target of rapamycin(mTOR)〖KG*4〗to promote the formation of autophagosome. In addition, the Baicalein can decrease alphasynuclein overexpression of nerve cell toxicity by reducing the release of cell lactate dehydrogenase.
〖HTH〗〖WTHZ〗Conclusion〖HTSS〗〓Autophagy activation induced by mTOR signal transduction pathway can lead to the removal of abnormal aggregation alphasynuclein in neurons.

Key words: Parkinson disease, Baicalein, autophagy