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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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 |
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© 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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Pinkaew D. Changtam C. Tocharus C. Govitrapong P. Jumnongprakhon P. Suksamrarn A. Tocharus J. |
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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. |
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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 |
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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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