@article {Mostafa:2016:0008-4212:699,
title = "The hydrogen sulfide releasing compounds ATB-346 and diallyl trisulfide attenuate streptozotocin-induced cognitive impairment, neuroinflammation, and oxidative stress in rats: involvement of asymmetric dimethylarginine",
journal = "Canadian Journal of Physiology and Pharmacology",
parent_itemid = "infobike://cndscipub/cjpp",
publishercode ="cndscipub",
year = "2016",
volume = "94",
number = "7",
publication date ="2016-01-01T00:00:00",
pages = "699-708",
itemtype = "ARTICLE",
issn = "0008-4212",
eissn = "1205-7541",
url = "https://www.ingentaconnect.com/content/cndscipub/cjpp/2016/00000094/00000007/art00003",
doi = "doi:10.1139/cjpp-2015-0316",
keyword = "hydrogen sulfide, neuroinflammation, stress oxydant, Alzheimer disease, ATB-346, oxidative stress, neuro-inflammation, maladie d’Alzheimer, sulfure d’hydrogène, et trisulfure de di-allyle, diallyl trisulfide, ATB-34",
author = "Mostafa, Dalia K. and El Azhary, Nesrine M. and Nasra, Rasha A.",
abstract = "Hydrogen sulfide (H2S) has attracted interest as a gaseous mediator involved in diverse processes in the nervous system, particularly with respect to learning and memory. However, its therapeutic potential in Alzheimer disease (AD) is not fully explored. Therefore, the effects
of H2S-releasing compounds against AD-like behavioural and biochemical abnormalities were investigated. Memory deficit was induced by intracerberoventicular injection of streptozotocin (STZ, 3 mg\textperiodcenteredkg1). Animals were randomly assigned into 5 groups (12 rats
each): normal control, STZ treated, and 3 drug-treated groups receiving naproxen, H2S-releasing naproxen (ATB-346), and diallyl trisulfide in 20, 32, 40 mg\textperiodcenteredkg1\textperiodcenteredday1, respectively. Memory function was assessed by passive avoidance
and T-maze tasks. After 21 days, hippocampal IL-6, malondialdehyde, reduced glutathione (GSH), asymmetric dimethylarginine (ADMA), and acetylcholinestrase activity were determined. ATB-346 and diallyl trisulfide ameliorated behavioural performance and reduced malondialdehyde, ADMA, and acetylcholinestrase
activity while increasing GSH. This study demonstrates the beneficial effects of H2S release in STZ-induced memory impairment by modulation of neuroinflammation, oxidative stress, and cholinergic function. It also delineates the implication of ADMA to the cognitive impairment induced
by STZ. These findings draw the attention to H2S-releasing compounds as new candidates for treating neurodegenerative disorders that have prominent oxidative and inflammatory components such as AD.",
}