A number of studies indicate that
free radicals are involved in the neurodegeneration in
Alzheimer's disease (AD). The role of
superoxide anion (O2*-) in neuronal cell injury induced by
reactive oxygen species (ROS) was examined in PC12 cells using
pyrogallol (1,2,3-benzenetrior), a donor to release O2*-.
Pyrogallol induced PC12 cell death at concentrations, which evidently increased intracellular O2*-, as assessed by O2*- sensitive fluorescent precursor
hydroethidine (HEt). A water extract of Curcuma longa L. (Zingiberaceae) (CLE), having O2*- scavenging activity rescued PC12 cells from
pyrogallol-induced cell death.
Hypoxia/reoxygenation injury of PC12 cells was also blocked by CLE. The present study was also conducted to examine the effect of CLE on H2O2 -induced toxicity in rat
pheochromocytoma line PC12 by measuring cell lesion, level of lipid peroxidation and
antioxidant enzyme activities. Following a 30 min exposure of the cells to H2O2 (150 microM), a marked decrease in cell survival, activities of
glutathione peroxidase and
catalase as well as increased production of
malondialdehyde (MDA) were found. Pretreatment of the cells with CLE (0.5-10 microg/ml) prior to H2O2 exposure significantly elevated the cell survival,
antioxidant enzyme activities and decreased the level of MDA. The above-mentioned
neuroprotective effects are also observed with
tacrine (THA, 1 microM), suggesting that the
neuroprotective effects of
cholinesterase inhibitor might partly contribute to the clinical efficacy in AD treatment. Further understanding of the underlying mechanism of the protective effects of these radical scavengers reducing intracellular O2*- on neuronal cell death may lead to development of new therapeutic treatments for hypoxic/ischemic
brain injury.