@article{ref1,
title="Protection from cyanide-induced brain injury by the Nrf2 transcriptional activator carnosic acid",
journal="Journal of neurochemistry",
year="2015",
author="Zhang, Dongxian and Lee, Brian and Nutter, Anthony and Song, Paul and Dolatabadi, Nima and Parker, James and Sanz-Blasco, Sara and Newmeyer, Traci and Ambasudhan, Rajesh and McKercher, Scott R. and Masliah, Eliezer and Lipton, Stuart A.",
volume="133",
number="6",
pages="898-908",
abstract="Cyanide is a life threatening, bioterrorist agent, preventing cellular respiration by inhibiting cytochrome c oxidase, resulting in cardiopulmonary failure, hypoxic brain injury, and death within minutes. However, even after treatment with various antidotes to protect cytochrome oxidase, cyanide intoxication in humans can induce a delayed-onset neurological syndrome that includes symptoms of Parkinsonism. Additional mechanisms are thought to underlie cyanide-induced neuronal damage, including generation of reactive oxygen species (ROS). This may account for the fact that antioxidants prevent some aspects of cyanide-induced neuronal damage. Here, as a potential preemptive countermeasure against a bioterrorist attack with cyanide, we tested the CNS protective effect of carnosic acid (CA), a pro-electrophilic compound found in the herb rosemary. CA crosses the blood-brain-barrier to upregulate endogenous antioxidant enzymes via activation of the Nrf2 transcriptional pathway. We demonstrate that CA exerts neuroprotective effects on cyanide-induced brain damage in cultured rodent and human induced pluripotent stem cell (hiPSC)-derived neurons in vitro, and in vivo in various brain areas of a non-Swiss albino (NSA) mouse model of cyanide poisoning that simulates damage observed in the human brain. This article is protected by copyright. All rights reserved.<p /><p>Language: en</p>",
language="en",
issn="0022-3042",
doi="10.1111/jnc.13074",
url="http://dx.doi.org/10.1111/jnc.13074"
}