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Eur J Pharmacol. 2017 Jan 15;795:13-21. doi: 10.1016/j.ejphar.2016.11.051. Epub 2016 Nov 30.

Garlic active constituent s-allyl cysteine protects against lipopolysaccharide-induced cognitive deficits in the rat: Possible involved mechanisms.

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School of Medicine, Shahed University, Tehran, Iran.
Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Neurophysiology Research Center, Shahed University, Tehran, Iran. Electronic address:
Neurophysiology Research Center, Shahed University, Tehran, Iran.
Neurophysiology Research Center, Shahed University, Tehran, Iran. Electronic address:


Neuroinflammation is known as a risk factor for cognitive deficit and dementia and its incidence increases with aging. S-allyl cysteine (SAC) is the active and main component of aged garlic extract with anti-inflammatory, neuroprotective, and nootropic potential. In this study, the protective effect of SAC against lipopolysaccharide (LPS)-induced cognitive deficit in the rat was investigated. For induction of learning and memory impairment and neuroinflammation, LPS was intraperitoneally injected at a dose of 167μg/kg for 7 days and SAC was administered p.o. at doses of 25, 50, or 100mg/kg/day, 30min after LPS, for seven days. Treatment of LPS-injected rats with SAC at a dose of 100mg/kg improved spatial recognition memory in Y maze, discrimination ratio in novel object discrimination task, and retention and recall in passive avoidance test. In addition, SAC at the latter dose mitigated lipid peroxidation marker malondialdehyde (MDA) and augmented key antioxidant defensive elements including superoxide dismutase (SOD), catalase and glutathione (GSH) in hippocampal homogenate and lowered acetylcholinesterase activity. Meanwhile, SAC down-regulated hippocampal nuclear factor-<kappa>B, toll-like receptor 4 (TLR4), glial fibrillary acidic protein (GFAP), and interleukin 1β (IL-1β) and up-regulated nuclear factor (erythroid-derived 2)-like 2 (Nrf2) in addition to lowering iba1-immunoreactive intensity in the hippocampus of LPS-injected group. Taken together, SAC administration could mitigate LPS-induced cognitive deficits via attenuation of oxidative stress, neuroinflammation, astrogliosis, and acetylcholinesterase activity.


Cognition; Learning and memory; Lipopolysaccharide; Neuroinflammation; S-allyl cysteine

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