Tanshinone IIA Inhibits Glutamate-Induced Oxidative Toxicity through Prevention of Mitochondrial Dysfunction and Suppression of MAPK Activation in SH-SY5Y Human Neuroblastoma Cells

Figure 6

Proposed mechanisms of action of tanshinone IIA against glutamate neurotoxicity. Excessive glutamate exposure induces a series of cytotoxic events including mitochondrial dysfunction and oxidative stress, leading to neuronal apoptosis. However, tanshinone IIA can promote neuronal survival and inhibit cell apoptosis through prevention of mitochondrial dysfunction, modulation of oxidative stress, and suppression of MAPK activation.