2018
DOI: 10.1016/j.toxlet.2018.02.002
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Acrylamide-induced oxidative stress and inflammatory response are alleviated by N-acetylcysteine in PC12 cells: Involvement of the crosstalk between Nrf2 and NF-κB pathways regulated by MAPKs

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Cited by 111 publications
(61 citation statements)
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“…In turn, increased ROS can lead to the oxidation of membrane lipids. Similar findings have been reported showing elevated serum malondialdehyde levels in rats after acrylamide treatment [36,37].…”
Section: Discussionsupporting
confidence: 90%
“…In turn, increased ROS can lead to the oxidation of membrane lipids. Similar findings have been reported showing elevated serum malondialdehyde levels in rats after acrylamide treatment [36,37].…”
Section: Discussionsupporting
confidence: 90%
“…Inflammatory factors such as TNF-α can promote the expression of inflammatory genes through mitogen activated protein kinases (MAPKs) cascade and NF-κB activation [95,96]. Therefore, inhibiting MAPKs and/or NF-κB pathway may significantly reduce the expression of inflammatory genes [97]. Aulakh et al [72] found that the inhibition of FAK expression may effectively inhibit vascular cell adhesion factor-1 (VCAM-1) expression.…”
Section: The Function Of Fak In Regulating Inflammation Pathwaymentioning
confidence: 99%
“…In particular, AA has been demonstrated to be neurotoxic in humans and laboratory animals [ 20 , 21 , 22 ], resulting in sensory and motor dysfunction, skeletal muscle weakness, weight loss, and ataxia [ 23 ]. One of the important mechanisms by which AA induces neurotoxicity is that it can destroy the redox balance and induce oxidative stress in neurons [ 24 , 25 ]. Under oxidative stress of AA, intracellular ROS were greatly produced, GSH levels decreased rapidly, and a series of oxidative stress followed [ 26 ].…”
Section: Discussionmentioning
confidence: 99%