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.