Journal of neurochemistry
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Journal of neurochemistry · Aug 2017
ReviewCholinesterase reactivators and bioscavengers for pre- and post-exposure treatments of organophosphorus poisoning.
Organophosphorus agents (OPs) irreversibly inhibit acetylcholinesterase (AChE) causing a major cholinergic syndrome. The medical counter-measures of OP poisoning have not evolved for the last 30 years with carbamates for pretreatment, pyridinium oximes-based AChE reactivators, antimuscarinic drugs and neuroprotective benzodiazepines for post-exposure treatment. These drugs ensure protection of peripheral nervous system and mitigate acute effects of OP lethal doses. ⋯ New therapeutic approaches for pre- and post-exposure treatments involve detoxification of OP molecules before they reach their molecular targets by administrating catalytic bioscavengers, among them phosphotriesterases are the most promising. Novel generation of broad spectrum reactivators are designed for crossing the blood-brain barrier and reactivate central AChE. This is an article for the special issue XVth International Symposium on Cholinergic Mechanisms.
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Journal of neurochemistry · Jul 2017
Endoplasmic reticulum stress mediates distinct impacts of sevoflurane on different subfields of immature hippocampus.
Sevoflurane, a typical inhaled anesthetic, is widely used in patients of all ages during surgery. The negative effects, such as inducing cell death and damaging spatial memory, of sevoflurane on neurodevelopment have raised increasing concerns in recent years. However, the molecular mechanism remains unclear. ⋯ Meanwhile, CA1 pyramidal neurons exhibited significantly reduced intrinsic excitability. Furthermore, the administration of ER stress inhibitor attenuated the above mentioned detrimental effects evidently and prevented the following relevant learning and memory deficits. In conclusion, sevoflurane-mediated ER stress performs distinct effects on the different subfields of the immature hippocampus and inhibiting ER stress during sevoflurane anesthesia will be a potential method to prevent the following learning and memory deficits in adulthood.
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Journal of neurochemistry · Jun 2017
RS9, a novel Nrf2 activator, attenuates light-induced death of cells of photoreceptor cells and Müller glia cells.
The retina is highly sensitive to oxidative stress because of its high consumption of oxygen associated with the phototransductional processes. Recent findings have suggested that oxidative stress is involved in the pathology of age-related macular degeneration, a progressive degeneration of the central retina. A well-known environmental risk factor is light exposure, as excessive and continuous light exposure can damage photoreceptors. ⋯ Heme oxygenase-1 was increased after light exposure, and Nrf2 was translocated into the nucleus after light exposure in vivo. Silencing of Ho-1 reduced the protective effects of RS9 against light-induced death of 661W cells. These findings indicate that RS9 has therapeutic potential for retinal diseases that are aggravated by light exposure.
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Journal of neurochemistry · Jun 2017
Dimercaprol is an acrolein scavenger that mitigates acrolein-mediated PC-12 cells toxicity and reduces acrolein in rat following spinal cord injury.
Acrolein is one of the most toxic byproducts of lipid peroxidation, and it has been shown to be associated with multiple pathological processes in trauma and diseases, including spinal cord injury, multiple sclerosis, and Alzheimer's disease. Therefore, suppressing acrolein using acrolein scavengers has been suggested as a novel strategy of neuroprotection. In an effort to identify effective acrolein scavengers, we have confirmed that dimercaprol, which possesses thiol functional groups, could bind and trap acrolein. ⋯ Its acrolein scavenging capability was further demonstrated by in vitro results that showed that dimercaprol could significantly protect PC-12 cells from acrolein-mediated cell death in a dose-dependent manner. Furthermore, dimercaprol, when applied systemically through intraperitoneal injection, could significantly reduce acrolein contents in spinal cord tissue following a spinal cord contusion injury in rats, a condition known to have elevated acrolein concentration. Taken together, dimercaprol may be an effective acrolein scavenger and a viable candidate for acrolein detoxification.
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Journal of neurochemistry · May 2017
Retraction Of PublicationRetraction Statement: CXCL12/CXCR4 chemokine signaling in spinal glia induces pain hypersensitivity through MAPKs-mediated neuroinflammation in bone cancer rats.
'CXCL12/CXCR4 chemokine signaling in spinal glia induces pain hypersensitivity through MAPKs-mediated neuroinflammation in bone cancer rats' by Hu X.-M., Liu Y.-N., Zhang H.-L., Cao S.-B., Zhang T., Chen L.-P. and Shen W. The above article from Journal of Neurochemistry, published online on 26 January 2015 and in volume 132, issue 4, pages 452-463 (available through www.onlinelibrary.wiley.com), and its subsequent Corrigendum, published online on 5 February 2015 and in volume 132, issue 4, p. 487, have been retracted by agreement between the Journal's Editor-in-Chief, Jörg Schulz, corresponding author Wen Shen on behalf of the authors, and John Wiley & Sons Ltd. The retraction has been agreed as the same GFAP immunostaining image was used to represent different experimental conditions in two different publications (Shen et al. [2014] in the Journal of Neuroinflammation and Hu et al. [2015] in the Journal of Neurochemistry), with apparent brightness changes between the images. ⋯ C. and Song C. (2014) CXCL12 in astrocytes contributes to bone cancer pain through CXCR4-mediated neuronal sensitization and glial activation in rat spinal cord. J. Neuroinflammation 11, 75. doi:10.1186/1742-2094-11-75.