Modulation of mitochondrial dysfunction in neurodegenerative diseases via activation of nuclear factor erythroid-2-related factor 2 by food-derived compounds

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• 作者：Isabel Denzer^a ; ^b ; ^{isabel.denzer@fau.de" class="auth_mail" title="E-mail the corresponding author} ; Gerald Mü ; nch^c ; ^d ; ^e ; ^{G.Muench@uws.edu.au" class="auth_mail" title="E-mail the corresponding author} ; Kristina Friedland^a ; ^{kristina.leuner@fau.de" class="auth_mail" title="E-mail the corresponding author}
• 关键词：3-NPA ; 3-nitropropionic acid ; 6-OHDA ; 6-hydroxy dopamine ; AD ; Alzheimer&rsquo ; s disease ; AIF ; apoptosis inducing factor ; ALS ; amyotrophic lateral sclerosis ; APP ; amyloid precursor protein ; Aß ; β-amyloid peptide ; CA ; trans-cinnamaldehyde ; Cat ; catalase ; CBP ; cAMP-response-element binding protein (CREB) binding protein ; CEppt ; aqueous cinnamon extract ; CGA ; chlorogenic acid (5-O-caffeoylquinic acid) ; CoQ ; coenzyme Q ; CREB ; cAMP-response-element binding protein ; C-SLNs ; curcumin encapsulated
• 刊名：Pharmacological Research
• 出版年：2016
• 出版时间：January 2016
• 年：2016
• 卷：103
• 期：Complete
• 页码：80-94
• 全文大小：2792 K

文摘

Oxidative stress and mitochondrial dysfunction are early events in the pathogenesis of neurodegenerative diseases, including Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD) and amyotrophic lateral sclerosis (ALS). Mitochondria are important key players in cellular function based on mitochondrial energy production and their major role in cell physiology. Since neurons are highly depending on mitochondrial energy production due to their high energy demand and their reduced glycolytic capacity mitochondrial dysfunction has fatal consequences for neuronal function and survival. The transcription factor nuclear factor erythroid-2-related factor 2 (Nrf2) is the major regulator of cellular response to oxidative stress. Activation of Nrf2 induces the transcriptional regulation of antioxidant response element (ARE)-dependent expression of a battery of cytoprotective and antioxidant enzymes and proteins. Moreover, activation of Nrf2 protects mitochondria from dysfunction and promotes mitochondrial biogenesis. Therefore, the Nrf2/ARE pathway has become an attractive target for the prevention and treatment of oxidative stress-related neurodegenerative diseases. Small food-derived inducers of the Nrf2/ARE pathway including l-sulforaphane from broccoli and isoliquiritigenin from licorice displayed promising protection of mitochondrial function in models of oxidative stress and neurodegenerative diseases and represent a novel approach to prevent and treat aging-associated neurodegenerative diseases.