Studies On The Protective Effect Of Salvianolic Acid B On The Mitochondrial Injury & Neuronal Apoptosis And Its Action Mechanisms

There are increasing evidences that mitochondria dysfunction and cellular apoptosis have been involved in the pathogenesis of many neuronal diseases, such as acute and chronic ischemia brain damage, Alzheimer's disease, Parkinson's disease, Huntington's disease. Mitochondria are not only the major source of energy metabolism, but also the source of superoxide anion production in cell. Furthermore, it has recently been proved that mitochondria play a role in regulating many apoptosis pathways. The mechanisms by which they exert apoptotic action include release of caspase activator (cytochrome C), disruption of oxidative phosphorylation, loss of mitochondria transmembrane potential, and formation of pro- or anti- apoptotic member of the Bcl-2 family. So effective mitochondria protective and antiapoptotic agents should be developed and be helpful in the therapy of a great deal of neuronal diseases.Salvianolic acid B (Sal B) is one of the water - soluble components isolated from a traditional Chinese drug - salvia miltiorrhiza. Previous experiments have found that it had potent antioxidative effects in vivo and in vitro. In this work, the models of mitochondria injured by focal cerebral reperfusion in rat and cellular apoptosis induced by 6-hydroxydopamine in caspase 3 overexpression PC 12 cell line were used. The protective effect of Salvianolic acid B on mitochondria injury & neuronal apoptosis and its...