Oroxylum indicum (L.) extract protects human neuroblastoma SH-SY5Y cells against ß-amyloid-induced cell injury

Nootchanat Mairuae, James R. Connor, Benjaporn Buranrat, Sang Y. Lee

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1933-1942
Number of pages10
JournalMolecular medicine reports
Volume20
Issue number2
DOIs
StatePublished - Jan 1 2019

Fingerprint

Oxidative stress
Neuroblastoma
Amyloid
Caspase 7
Caspase 3
Oxidative Stress
Reactive Oxygen Species
Wounds and Injuries
Catalase
Superoxide Dismutase
Carrier Proteins
Cells
Neurodegenerative diseases
Cell Survival
Alzheimer Disease
Phosphorylation
L-Lactate Dehydrogenase
Amyloid Plaques
Neurodegenerative Diseases
Up-Regulation

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Medicine
  • Molecular Biology
  • Genetics
  • Oncology
  • Cancer Research

Cite this

@article{210590d67c194e469adfeec31eac7539,
title = "Oroxylum indicum (L.) extract protects human neuroblastoma SH-SY5Y cells against {\ss}-amyloid-induced cell injury",
abstract = "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 A{\ss}25-35-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 A{\ss}25-35 significantly increased cellular oxidative stress, as evidenced by the increased ROS levels. A{\ss}25-35 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 A{\ss}25-35 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 A{\ss}25-35-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 A{\ss} in AD and related neurodegenerative diseases. Further studies investigating the activity of Oroxylum indicum extract in vivo are now required.",
author = "Nootchanat Mairuae and Connor, {James R.} and Benjaporn Buranrat and Lee, {Sang Y.}",
year = "2019",
month = "1",
day = "1",
doi = "10.3892/mmr.2019.10411",
language = "English (US)",
volume = "20",
pages = "1933--1942",
journal = "Molecular Medicine Reports",
issn = "1791-2997",
publisher = "Spandidos Publications",
number = "2",

}

Oroxylum indicum (L.) extract protects human neuroblastoma SH-SY5Y cells against ß-amyloid-induced cell injury. / Mairuae, Nootchanat; Connor, James R.; Buranrat, Benjaporn; Lee, Sang Y.

In: Molecular medicine reports, Vol. 20, No. 2, 01.01.2019, p. 1933-1942.

Research output: Contribution to journalArticle

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.

PY - 2019/1/1

Y1 - 2019/1/1

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.

UR - http://www.scopus.com/inward/record.url?scp=85068678044&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85068678044&partnerID=8YFLogxK

U2 - 10.3892/mmr.2019.10411

DO - 10.3892/mmr.2019.10411

M3 - Article

C2 - 31257498

AN - SCOPUS:85068678044

VL - 20

SP - 1933

EP - 1942

JO - Molecular Medicine Reports

JF - Molecular Medicine Reports

SN - 1791-2997

IS - 2

ER -