Neuropharmacological Potential of Gastrodia elata Blume and Its Components

Figure 5

Schematic representation of the neuropharmacological effects of Gastrodia elata (GE). Multiple disease mechanisms, such as neurotransmitter imbalance, oxidative damage, and neuroinflammation, reportedly induce a variety of neurodegenerative disorders. GE has the potential to positively restore the neuronal cell damage in neurodegenerative diseases via the upregulation of inhibitory neurotransmitters and downregulation of oxidative stress and neuroinflammation. ASK-1: apoptosis signal-regulating kinase-1; CaMKII: Ca²⁺/calmodulin-dependent kinase II; COX-2: cyclooxygenase-2; GABA-T: gamma aminobutyric acid transaminase; GAD: glutamate decarboxylase; GE: Gastrodia elata; iNOS: inducible nitric oxide synthase; JNK: c-jun N-terminal kinases; MAPK: mitogen-activated protein kinase; NO: nitric oxide; SOD: superoxide dismutase; SSADH: succinic semialdehyde dehydrogenase.