2020
DOI: 10.1016/j.neuropharm.2020.107989
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Nrf2 activator via interference of Nrf2-Keap1 interaction has antioxidant and anti-inflammatory properties in Parkinson's disease animal model

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Cited by 78 publications
(51 citation statements)
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“…Furthermore, oxidative stress stimulates the activation of the redox-sensitive transcription factors, which in turn manages the expression of pro-inflammatory mediators. The Nrf2 and NF-kB pathway are closely related in the oxidative stress [ 41 ] and inflammatory [ 42 ] answers, respectively. They are transcription factors usually localized in the cytosol and regulated by Kelch-like ECH-associated protein 1 (Keap1) and IκBα inhibitor, respectively.…”
Section: Discussionmentioning
confidence: 99%
“…Furthermore, oxidative stress stimulates the activation of the redox-sensitive transcription factors, which in turn manages the expression of pro-inflammatory mediators. The Nrf2 and NF-kB pathway are closely related in the oxidative stress [ 41 ] and inflammatory [ 42 ] answers, respectively. They are transcription factors usually localized in the cytosol and regulated by Kelch-like ECH-associated protein 1 (Keap1) and IκBα inhibitor, respectively.…”
Section: Discussionmentioning
confidence: 99%
“…The brains of 5 mice for each group were fixed, cut and colored with hematoxylin and eosin (H&E, Bio-Optica, Milan, Italy) and subsequently the sections were analyzed using an optical microscope connected to an imaging system (AxioVision, Zeiss, Milan, Italy), as previously described [ 30 , 35 ]. Histopathological evaluation was performed blindly using a semi-quantitative five point rating: 0 = normal, no death neuron observed; 1 = insignificant pathology, SN contained one to five death neurons; 2 = modest pathology, SN contained five to 10 death neurons; 3 = severe pathology, SN contained more than 10 death neurons; 4 = more severe pathology, SN contained only death neurons [ 48 ].…”
Section: Methodsmentioning
confidence: 99%
“…Recently, increasing evidence reports that HT and its derivates activate the phase 2 response, leading to the expression of the nuclear factor erythroid 2-related factor (Nrf2) antioxidant pathway [ 27 , 28 ]. Interestingly, Nrf2 represents a crucial mechanism of resistance to oxidative stress and inflammation in vitro and in vivo [ 29 , 30 ]. In line with these observations, Nrf2 codifies the antioxidant pathway of vitagenes, which exist to counteract various forms of stress (e.g., oxidative, environmental and proteotoxic stress).…”
Section: Introductionmentioning
confidence: 99%
“…Thus, the expression of human α-synuclein in the ventral midbrain of Nrf2-deficient mice leads to degeneration of nigral dopaminergic neurons and increased dystrophic dendrites, reminiscent of Lewy neurites; this neuronal loss is associated with neuroinflammation and gliosis. 123 Nrf2-deficient mice are also much more sensitive to the neurotoxic effects of MPTP than their wild-type counterparts, whereas Nrf2 activation has neuroprotective effects in Nrf2-wildtype, but not Nrf2-deficient mice in this model of PD, [124][125][126][127][128][129][130] as well as in mice expressing human α-synuclein. 94 In both models, these protective effects are associated with a decrease in oxidative damage and neuroinflammation.…”
Section: Targeting Nrf2 In Mitochondrial Dysfunction In Pdmentioning
confidence: 93%