Association of Neuroprotective Effect of Di-O-Demethylcurcumin on Aβ<inf>25–35</inf>-Induced Neurotoxicity with Suppression of NF-κB and Activation of Nrf2

© 2015, Springer Science+Business Media New York. Amyloid-β peptides (Aβ), a major component of senile plaques, play an important role in the development and progression of Alzheimer’s disease. Several lines of evidence have demonstrated that Aβ-induced neuronal death is mediated by oxidative stress...

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Main Authors: Pinkaew D., Changtam C., Tocharus C., Govitrapong P., Jumnongprakhon P., Suksamrarn A., Tocharus J.
Format: Journal
Published: 2017
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http://cmuir.cmu.ac.th/jspui/handle/6653943832/42536
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spelling th-cmuir.6653943832-425362017-09-28T04:27:40Z Association of Neuroprotective Effect of Di-O-Demethylcurcumin on Aβ<inf>25–35</inf>-Induced Neurotoxicity with Suppression of NF-κB and Activation of Nrf2 Pinkaew D. Changtam C. Tocharus C. Govitrapong P. Jumnongprakhon P. Suksamrarn A. Tocharus J. © 2015, Springer Science+Business Media New York. Amyloid-β peptides (Aβ), a major component of senile plaques, play an important role in the development and progression of Alzheimer’s disease. Several lines of evidence have demonstrated that Aβ-induced neuronal death is mediated by oxidative stress. The present study aimed to evaluate the potential involvement of di-O-demethylcurcumin, an analog of curcuminoid, on Aβ-induced neurotoxicity in culture neuroblastoma cells (SK-N-SH cells) through the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway and the suppression of nuclear factor-κB (NF-κB) signaling pathway and their downstream targets. The results showed that pretreatment with di-O-demethylcurcumin elevated cell viability and decreased the level of reactive oxygen species. Moreover, treatment with di-O-demethylcurcumin promoted the translocation of Nrf2 protein from the cytoplasm to the nucleus, increased the expression of Nrf2-ARE pathway-related downstream proteins including heme oxygenase (HO-1) , NAD(P)H:quinone oxidoreductase 1 and glutamate-cysteine ligase catalytic subunit, and increased the activity of superoxide dismutase enzymes. On the other hand, di-O-demethylcurcumin suppressed the degradation of IκBα, translocation of the p65 subunit of NF-κB from cytoplasm to nucleus and thereby, attenuated the expression of inducible nitric oxide synthase protein and nitric oxide production. Taken together, these results suggest that neuroinflammatory effect of di-O-demethylcurcumin might potentially be due to inhibit NF-κB and activate Nrf2 signaling pathways induced by Aβ 25–35 . 2017-09-28T04:27:40Z 2017-09-28T04:27:40Z 2016-01-01 Journal 10298428 2-s2.0-84953347339 10.1007/s12640-015-9558-4 https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84953347339&origin=inward http://cmuir.cmu.ac.th/jspui/handle/6653943832/42536
institution Chiang Mai University
building Chiang Mai University Library
country Thailand
collection CMU Intellectual Repository
description © 2015, Springer Science+Business Media New York. Amyloid-β peptides (Aβ), a major component of senile plaques, play an important role in the development and progression of Alzheimer’s disease. Several lines of evidence have demonstrated that Aβ-induced neuronal death is mediated by oxidative stress. The present study aimed to evaluate the potential involvement of di-O-demethylcurcumin, an analog of curcuminoid, on Aβ-induced neurotoxicity in culture neuroblastoma cells (SK-N-SH cells) through the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway and the suppression of nuclear factor-κB (NF-κB) signaling pathway and their downstream targets. The results showed that pretreatment with di-O-demethylcurcumin elevated cell viability and decreased the level of reactive oxygen species. Moreover, treatment with di-O-demethylcurcumin promoted the translocation of Nrf2 protein from the cytoplasm to the nucleus, increased the expression of Nrf2-ARE pathway-related downstream proteins including heme oxygenase (HO-1) , NAD(P)H:quinone oxidoreductase 1 and glutamate-cysteine ligase catalytic subunit, and increased the activity of superoxide dismutase enzymes. On the other hand, di-O-demethylcurcumin suppressed the degradation of IκBα, translocation of the p65 subunit of NF-κB from cytoplasm to nucleus and thereby, attenuated the expression of inducible nitric oxide synthase protein and nitric oxide production. Taken together, these results suggest that neuroinflammatory effect of di-O-demethylcurcumin might potentially be due to inhibit NF-κB and activate Nrf2 signaling pathways induced by Aβ 25–35 .
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author Pinkaew D.
Changtam C.
Tocharus C.
Govitrapong P.
Jumnongprakhon P.
Suksamrarn A.
Tocharus J.
spellingShingle Pinkaew D.
Changtam C.
Tocharus C.
Govitrapong P.
Jumnongprakhon P.
Suksamrarn A.
Tocharus J.
Association of Neuroprotective Effect of Di-O-Demethylcurcumin on Aβ<inf>25–35</inf>-Induced Neurotoxicity with Suppression of NF-κB and Activation of Nrf2
author_facet Pinkaew D.
Changtam C.
Tocharus C.
Govitrapong P.
Jumnongprakhon P.
Suksamrarn A.
Tocharus J.
author_sort Pinkaew D.
title Association of Neuroprotective Effect of Di-O-Demethylcurcumin on Aβ<inf>25–35</inf>-Induced Neurotoxicity with Suppression of NF-κB and Activation of Nrf2
title_short Association of Neuroprotective Effect of Di-O-Demethylcurcumin on Aβ<inf>25–35</inf>-Induced Neurotoxicity with Suppression of NF-κB and Activation of Nrf2
title_full Association of Neuroprotective Effect of Di-O-Demethylcurcumin on Aβ<inf>25–35</inf>-Induced Neurotoxicity with Suppression of NF-κB and Activation of Nrf2
title_fullStr Association of Neuroprotective Effect of Di-O-Demethylcurcumin on Aβ<inf>25–35</inf>-Induced Neurotoxicity with Suppression of NF-κB and Activation of Nrf2
title_full_unstemmed Association of Neuroprotective Effect of Di-O-Demethylcurcumin on Aβ<inf>25–35</inf>-Induced Neurotoxicity with Suppression of NF-κB and Activation of Nrf2
title_sort association of neuroprotective effect of di-o-demethylcurcumin on aβ<inf>25–35</inf>-induced neurotoxicity with suppression of nf-κb and activation of nrf2
publishDate 2017
url https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84953347339&origin=inward
http://cmuir.cmu.ac.th/jspui/handle/6653943832/42536
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