Effect of Tacrine‐3‐caffeic Acid, A Novel Multifunctional Anti‐Alzheimer's Dimer, Against Oxidative‐Stress‐Induced Cell Death in <scp>HT</scp>22 Hippocampal Neurons: Involvement of Nrf2/<scp>HO</scp>‐1 Pathway

Chao, Xiaojuan; Chen, Zi-Wei; Liu, Anmin; He, Xian-Hui; Wang, Shao-Gui; Wang, Yuting; Liu, Peiqing; Ramassamy, Charles; Mak, Shinghung; Cui, Wei; Kong, Ah‐Ng Tony; Yu, Zujiang; Han, Yifan; Pi, Rongbiao

doi:10.1111/cns.12286

Cited by 49 publications

(33 citation statements)

References 62 publications

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“…This indicates that elevation of HO-1 level is not the primary factor contributing to its acute protective effect. These data are similar to those from previous studies showing the time course of increased expression of SOD2 and HO-1 (Chao et al, 2014) in response to other polyphenols, suggesting that this temporal profile is a generalizable phenomenon. For simultaneous treatment of HT-22 cells with glutamate and tBHQ, both SOD2 and HO-1 expression were increased before cell death, which allows either or both to protect cells.…”

Section: Discussionsupporting

confidence: 90%

“…This indicates that, within 3 hours after application, tBHQ efficiently maintains mitochondrial function and further prevents cell damage. Upregulation of HO-1 expression has been shown to prevent glutamate-induced oxidative toxicity in HT-22 cells (Rössler et al, 2004;Son et al, 2013;Chao et al, 2014). However, the temporal profile of expression of SOD2 and HO-1 shows that peak SOD2 expression occurs at 3 hours but HO-1 expression does not peak until 12 hours following exposure to tBHQ (Fig.…”

Section: Discussionmentioning

confidence: 96%

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Sequential Upregulation of Superoxide Dismutase 2 and Heme Oxygenase 1 by tert-Butylhydroquinone Protects Mitochondria during Oxidative Stress

2015

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Oxidative stress is linked to mitochondrial dysfunction in aging and neurodegenerative conditions. The transcription factor nuclear factor E2-related factor 2 (Nrf2)-antioxidant response element (ARE) regulates intracellular antioxidative capacity to combat oxidative stress. We examined the effect of tertbutylhydroquinone (tBHQ), an Nrf2-ARE signaling pathway inducer, on mitochondrial function during oxidative challenge in neurons. tBHQ prevented glutamate-induced cytotoxicity in an HT-22 neuronal cell line even with an 8-hour exposure delay. tBHQ blocked glutamate-induced intracellular reactive oxygen species (ROS) and mitochondrial superoxide accumulation. It also protected mitochondrial function under glutamate toxicity, including maintaining mitochondrial membrane potential, mitochondrial Ca 21 hemostasis, and mitochondrial respiration. Glutamate-activated, mitochondria-mediated apoptosis was inhibited by tBHQ as well. In rat primary cortical neurons, tBHQ protected cells from both glutamate and buthionine sulfoximine toxicity. We found that tBHQ scavenged ROS and induced a rapid upregulation of superoxide dismutase 2 (SOD2) expression and a delayed upregulation of heme oxygenase 1 (HO-1) expression. In HT-22 cells with a knockdown of SOD2 expression, delayed treatment with tBHQ failed to prevent glutamate-induced cell death. Briefly, tBHQ rescues mitochondrial function by sequentially increasing SOD2 and HO-1 expression during glutamate-mediated oxidative stress. This study is the first to demonstrate the role of tBHQ in preserving mitochondrial function during oxidative challenge and provides a clinically relevant argument for using tBHQ against acute neuron-compromising conditions.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 96%

Sequential Upregulation of Superoxide Dismutase 2 and Heme Oxygenase 1 by tert-Butylhydroquinone Protects Mitochondria during Oxidative Stress

2015

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“…In an earlier study decreased NF-kB activation was detected in brusatoltreated HL-60 cells when exposed to significantly higher (micromolar) concentrations [2]. An inhibitory effect of brusatol on the transcription factor Nrf2 is well established and has been demonstrated in cell lines such as A549, HT22, Hepa-1c1c7 [3,14,15], and in bTC6 (our unpublished data). Nevertheless, Nrf2 downregulation is unlikely to mediate the anti-iNOS activity of brusatol since the Keap1/Nrf2 system is not implicated in regulation of iNOS expression.…”

Section: Discussionsupporting

confidence: 53%

Brusatol inhibits the response of cultured beta-cells to pro-inflammatory cytokines in vitro

Turpaev

Welsh

2015

Biochemical and Biophysical Research Communications

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Citation for the original published paper (version of record):Turpaev, K., Welsh, N. (2015) Brusatol inhibits the response of cultured beta-cells to pro-inflammatory cytokines in vitro. Brusatol is a natural terpenoid that is capable of inducing a variety of biological effects. We 19 presently report that this substance dramatically improves beta-cell survival when exposed to Biochemical and Biophysical

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“…Furthermore, CDDOmethylamide, a potent activator of Nrf2 signaling, significantly improves spatial memory retention and reduces plaque burden, Ab 1-42 levels, microgliosis and oxidative stress in Tg19959 mice, which carry the human amyloid precursor protein with two mutations [22]. Recently, Chao et al [23] reported that tacrine-3-caffeic acid, a novel promising multifunctional dimer against AD, could protect neurons against glutamate-induced cell death partially through Nrf2/ARE/HO-1 signaling pathway. These studies support a protective role of Nrf2 pathway in AD cellular and animal models and provide an emerging avenue for the treatment of AD.…”

Section: Discussionmentioning

confidence: 99%

Eriodictyol Attenuates β-Amyloid 25–35 Peptide-Induced Oxidative Cell Death in Primary Cultured Neurons by Activation of Nrf2

Shi

Zhu³

et al. 2015

Neurochem Res

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Oxidative stress plays an important role in the pathogenesis of neurodegenerative diseases, including Alzheimer's disease (AD). Eriodictyol, a flavonoid isolated from the Chinese herb Dracocephalum rupestre, has long been established as an antioxidant. The present study was designed to investigate the effect of eriodictyol on β-amyloid 25-35 peptide (Aβ25-35)-induced oxidative cell death in primary neurons and to explore the role of the nuclear factor erythroid-2-related factor 2/antioxidant response element (Nrf2/ARE) pathway in this process. For this purpose, primary cultures of cortical neurons were exposed to 15 μM Aβ25-35 in the absence or presence of eriodictyol (20, 40 and 80 μM). The results revealed that Aβ25-35-induced cytotoxicity and apoptotic characteristics such as activation of JNK/p38 apoptotic signaling pathway were effectively attenuated by eriodictyol pretreatment. Eriodictyol treatment also resulted in an increase in Nrf2 protein levels and subsequent activation of ARE pathway genes in primary cultured neurons. The protective effects of eriodictyol were attenuated by RNA interference-mediated knockdown of Nrf2 expression. Taken together, these results clearly demonstrate that eriodictyol protects neurons against Aβ25-35-induced cell death partially through Nrf2/ARE signaling pathway, which further supports that eriodictyol might be a promising novel therapeutic agent for AD.

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Effect of Tacrine‐3‐caffeic Acid, A Novel Multifunctional Anti‐Alzheimer's Dimer, Against Oxidative‐Stress‐Induced Cell Death in HT22 Hippocampal Neurons: Involvement of Nrf2/HO‐1 Pathway

Abstract: Taken together, these results clearly demonstrate that T3CA protects neurons against OS-induced cell death partially through Nrf2/ARE/HO-1 signaling pathway, which further supports that T3CA might be a promising novel therapeutic agent for OS-associated diseases.

Cited by 49 publications

References 62 publications

Sequential Upregulation of Superoxide Dismutase 2 and Heme Oxygenase 1 by tert-Butylhydroquinone Protects Mitochondria during Oxidative Stress

Sequential Upregulation of Superoxide Dismutase 2 and Heme Oxygenase 1 by tert-Butylhydroquinone Protects Mitochondria during Oxidative Stress

Brusatol inhibits the response of cultured beta-cells to pro-inflammatory cytokines in vitro

Eriodictyol Attenuates β-Amyloid 25–35 Peptide-Induced Oxidative Cell Death in Primary Cultured Neurons by Activation of Nrf2

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