TY - JOUR
T1 - Oroxylum indicum (L.) extract protects human neuroblastoma SH-SY5Y cells against ß-amyloid-induced cell injury
AU - Mairuae, Nootchanat
AU - Connor, James R.
AU - Buranrat, Benjaporn
AU - Lee, Sang Y.
N1 - Funding Information:
This study was financially supported by a grant from Mahasarakham university Faculty of Medicine and George M. leader Family Funds.
Publisher Copyright:
© 2019 Spandidos Publications. All rights reserved.
PY - 2019
Y1 - 2019
N2 - It has been reported that amyloid ß peptide, the major component of senile plaques, serves a critical role in the development and progression of Alzheimer's disease (AD) by generating reactive oxygen species (ROS), leading to oxidative stress. The aim of the present study was to inves¬ tigate the protective effect of Oroxylum indicum (L.) extract against Aß25-35-induced oxidative stress and cell injury using SH-SY5Y cells as a model, and at exploring the Underlying mechanisms. The results revealed that the exposure of cells to 20 piM Aß25-35 significantly increased cellular oxidative stress, as evidenced by the increased ROS levels. Aß25-35 treatment also increased caspase-3/7 activity and lactate dehydrogenase (LDH) release, and caused viability loss. Oroxylum indicum treatment not only attenuated the generation of ROS and suppressed caspase-3/7 activity but also reduced the neurotoxicity of Aß25-35 in a concentration-dependent manner, as evidenced by the increased cell viability and decreased L D H release. Treatment with Oroxylum indicum also increased superoxide dismutase (SOD) and catalase (CAT) activity, increased the phosphorylation of Akt and cAMP-responsive element binding protein (CREB), and contributed to the upregulation of Bcl-2 protein. In combina¬ tion, these results indicated that Oroxylum indicum extract could protect SH-SY5Y cells against Aß25-35-induced cell injury, at least partly, by inhibiting oxidative stress, increasing SOD and CAT activity, attenuating caspase 3/7 activity and promoting the cell survival pathway, Akt/CREB/Bcl-2. The approach used in the present study may also be useful for preventing the neurotoxicity induced by Aß in AD and related neurodegenerative diseases. Further studies investigating the activity of Oroxylum indicum extract in vivo are now required.
AB - It has been reported that amyloid ß peptide, the major component of senile plaques, serves a critical role in the development and progression of Alzheimer's disease (AD) by generating reactive oxygen species (ROS), leading to oxidative stress. The aim of the present study was to inves¬ tigate the protective effect of Oroxylum indicum (L.) extract against Aß25-35-induced oxidative stress and cell injury using SH-SY5Y cells as a model, and at exploring the Underlying mechanisms. The results revealed that the exposure of cells to 20 piM Aß25-35 significantly increased cellular oxidative stress, as evidenced by the increased ROS levels. Aß25-35 treatment also increased caspase-3/7 activity and lactate dehydrogenase (LDH) release, and caused viability loss. Oroxylum indicum treatment not only attenuated the generation of ROS and suppressed caspase-3/7 activity but also reduced the neurotoxicity of Aß25-35 in a concentration-dependent manner, as evidenced by the increased cell viability and decreased L D H release. Treatment with Oroxylum indicum also increased superoxide dismutase (SOD) and catalase (CAT) activity, increased the phosphorylation of Akt and cAMP-responsive element binding protein (CREB), and contributed to the upregulation of Bcl-2 protein. In combina¬ tion, these results indicated that Oroxylum indicum extract could protect SH-SY5Y cells against Aß25-35-induced cell injury, at least partly, by inhibiting oxidative stress, increasing SOD and CAT activity, attenuating caspase 3/7 activity and promoting the cell survival pathway, Akt/CREB/Bcl-2. The approach used in the present study may also be useful for preventing the neurotoxicity induced by Aß in AD and related neurodegenerative diseases. Further studies investigating the activity of Oroxylum indicum extract in vivo are now required.
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U2 - 10.3892/mmr.2019.10411
DO - 10.3892/mmr.2019.10411
M3 - Article
C2 - 31257498
AN - SCOPUS:85068678044
SN - 1791-2997
VL - 20
SP - 1933
EP - 1942
JO - Molecular medicine reports
JF - Molecular medicine reports
IS - 2
ER -