Garlic active constituents S-allylcysteine protects against lipopolysaccharide-induced cognitive deficit in the rat :possible involved mechnism

Mahboubeh Zare Zadeh Afshinmajd          Mehrdad Roghani

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URL :   http://research.shahed.ac.ir/WSR/WebPages/Report/PaperView.aspx?PaperID=43276
Date :  2017/01/30
Publish in :    European Journal of Pharmacology

Link :  http://dx.doi.org/10.1016/j.ejphar.2016.11.051
Keywords :Garlic, constituents, protects, lipopolysaccharide-induced, cognitive, possible, involved

Abstract :

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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 167 μg/kg for 7 days and SAC was administered p.o. at doses of 25, 50, or 100 mg/kg/day, 30 min after LPS, for seven days. Treatment of LPSinjected rats with SAC at a dose of 100 mg/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 LPSinduced cognitive deficits via attenuation of oxidative stress, neuroinflammation, astrogliosis, and acetylcholinesterase activity.