Biol. Pharm. Bull. 28(6) 1016—1020 (2005)

ing disability and therefore neural cell survival is a concern in aging brains as well as in many diseases of the central nervous system (CNS). Ischemic stroke results from a transient or permanent reduction in cerebral blood flow that is restricted to the territory of a major brain artery. The reduction in flow is, in most cases, caused by the occlusion of a cerebral artery either by an embolus or by local thrombosis. Transient focal cerebral ischemia initiates a cascade of detrimental events including accumulation of intracellular Ca and formation of free radicals. When blood flow is restored, oxygen can enhance the biochemical reactions that generate free radicals. The formation of free radicals also plays an important role in the pathogenesis of ischemic cell damage. Free radicals damage the lipid constituents of cellular and organelle membranes, which leads to neuronal death. This cell death can be divided into two broad categories: early necrotic death of cells in the ischemic core and delayed death of susceptible neurons in other neighboring regions, the socalled penumbra. Because the second category of cellular death occurs over an extended time, these neurons have the potential to be rescued by pharmacologic agents. Gastrodia elata blume (GEB) is a traditional herbal agent that has been used as an anticonvulsant, analgesic, and sedative to treat general paralysis, epilepsy, vertigo, and tetanus in Oriental countries for centuries. An earlier study showed that GEB can reduce lipid peroxide levels and has free radical-scavenging activities in rats with ferric chlorideinduced seizure. The results also suggested that these effects of GEB result mainly from the action of its major components, vanillin and p-hydroxybenzyl alcohol (HBA). The aqueous extract of GEB improved D-galactose-induced memory impairment in mice and performance deficits in senescent mice on the step-down passive avoidance task. Recently, it has been reported that compounds found in GEB inhibit glutamate-induced apoptosis in neuronal cells. Additionally, after pentylenetetrazole induced seizure activity, the ether fraction of GEB has been shown to attenuate the decrease in g-aminobutyric acid (GABA) and the increase in glutamate content, as well as to have anticonvulsant effects. Compounds in the ethyl ether fraction of GEB dramatically reduce the extent of neuronal cell death in IMR-32 neuroblastoma cells treated with amyloid-beta peptide. The improving effect of HBA after acute administration on learning and memory processes might be related to the decrease in dopamine concentration or other monoamine concentration and prevent DNA degradation. HBA isolated from the ethyl acetate fraction of the methanol extract also significantly prolonged the shortened step-through latency induced by scopolamine in the passive avoidance task. Exposure of tissues to oxygen free radicals results in lipid peroxidation, protein oxidation, and DNA damage. The final result induced by these oxidatively damaged macromolecules is to give rise to neurodegeneration. Therefore it appeared to be important to investigate the expression level of antioxidant proteins in brain disease. It was reported that protein disulfide isomerase (PDI) serves as a repair system for oxidatively damaged proteins via reduction of oxidized thiols in vascular endothelial cells. Upregulated PDI may play a critical role in resistance to ischemic damage, and the elevation of levels of this protein in the brain may have beneficial effects in brain stroke. The 1-Cys peroxiredoxin (1-Cys Prx) protein 1016 Biol. Pharm. Bull. 28(6) 1016—1020 (2005) Vol. 28, No. 6