TY - JOUR
T1 - Curcumin protected PC12 cells against beta-amyloid-induced toxicity through the inhibition of oxidative damage and tau hyperphosphorylation
AU - Park, So Young
AU - Kim, Hyo Shin
AU - Cho, Eun Kyung
AU - Kwon, Bo Youn
AU - Phark, Sohee
AU - Hwang, Kwang Woo
AU - Sul, Donggeun
N1 - Funding Information:
This research was supported by the Grant of Medical Research Center for Environmental Toxico-Genomics & Proteomics, funded by Korea Science and Engineering Foundations and Ministry of Science & Technology.
PY - 2008/8
Y1 - 2008/8
N2 - One of the pathological hallmarks of Alzheimer's disease is the progressive accumulation of beta-amyloid (Aβ) in the form of senile plaques, and Aβ insult to neuronal cells has been identified as one of the major causes of the onset of the disease. Curcumin, the major and most active antioxidant of Curcuma longa, protects neuronal cells against Aβ-induced toxicity. Therefore, in this study, we investigated the neuroprotective mechanisms by which curcumin acts against Aβ (25-35)-induced toxicity in PC12 cells. Following the exposure of PC12 cells to 10 μM Aβ (25-35) for 24 h, significant increases in the level of antioxidant enzymes, and DNA damage were observed, and these increases were accompanied by a decrease in cell viability, and an increase in intracellular calcium levels and tau hyperphosphorylation. In addition, pretreatment of PC12 cells with 10 μg/ml curcumin for 1 h significantly reversed the effect of Aβ, by decreasing the oxidative stress, and DNA damage induced by Aβ, as well as attenuating the elevation of intracellular calcium levels and tau hyperphosphorylation induced by Aβ. Taken together, these data indicate that curucmin protected PC12 cells against Aβ-induced neurotoxicity through the inhibition of oxidative damage, intracellular calcium influx, and tau hyperphosphorylation.
AB - One of the pathological hallmarks of Alzheimer's disease is the progressive accumulation of beta-amyloid (Aβ) in the form of senile plaques, and Aβ insult to neuronal cells has been identified as one of the major causes of the onset of the disease. Curcumin, the major and most active antioxidant of Curcuma longa, protects neuronal cells against Aβ-induced toxicity. Therefore, in this study, we investigated the neuroprotective mechanisms by which curcumin acts against Aβ (25-35)-induced toxicity in PC12 cells. Following the exposure of PC12 cells to 10 μM Aβ (25-35) for 24 h, significant increases in the level of antioxidant enzymes, and DNA damage were observed, and these increases were accompanied by a decrease in cell viability, and an increase in intracellular calcium levels and tau hyperphosphorylation. In addition, pretreatment of PC12 cells with 10 μg/ml curcumin for 1 h significantly reversed the effect of Aβ, by decreasing the oxidative stress, and DNA damage induced by Aβ, as well as attenuating the elevation of intracellular calcium levels and tau hyperphosphorylation induced by Aβ. Taken together, these data indicate that curucmin protected PC12 cells against Aβ-induced neurotoxicity through the inhibition of oxidative damage, intracellular calcium influx, and tau hyperphosphorylation.
KW - Beta-amyloid
KW - Calcium influx
KW - Curcumin
KW - Oxidative stress
KW - Tau hyperphosphorylation
UR - http://www.scopus.com/inward/record.url?scp=47349123450&partnerID=8YFLogxK
U2 - 10.1016/j.fct.2008.05.030
DO - 10.1016/j.fct.2008.05.030
M3 - Article
C2 - 18573304
AN - SCOPUS:47349123450
SN - 0278-6915
VL - 46
SP - 2881
EP - 2887
JO - Food and Chemical Toxicology
JF - Food and Chemical Toxicology
IS - 8
ER -