Figure 2.

A proposed mechanism of neuroprotection by BBR against oxidative stress, mitochondrial dysfunction, and apoptosis. ↑ indicates the upregulation by BBR; ↓ indicates the downregulation by BBR. PI3K, phosphoinositide 3-kinase; Akt, protein kinase B; GSK3β, glycogen synthase kinase 3β; ERK1/2, extracellular regulated protein kinases 1/2; PPAR, peroxisome proliferators-activated receptor; Nrf2, nuclear factor-E2-related factor 2; HO-1, heme oxygenase-1; NQO1, NAD (P)H quinone oxidoreductase 1; NMDAR1, N-methyl-d-aspartate receptor 1; NOX3, NADPH oxidase 3; ROS, reactive oxygen species; JNK, c-Jun N-terminal kinase; ATP, adenosine triphosphate; SOD, superoxide dismutase; GSH-PX, glutathione peroxidase; CAT, catalase; CytC, cytochrome c; AIF, apoptosis-inducing factor; Bax, Bcl-2-associated X protein; Bcl2, B-cell lymphoma-2; Bcl-XL, B-cell lymphoma-extra-large.