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KMID : 0606920140220010017
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Biomolecules & Therapeutics
2014 Volume.22 No. 1 p.17 ~ p.26
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α-Asarone Ameliorates Memory Deficit in Lipopolysaccharide-Treated Mice via Suppression of Pro-Inflammatory Cytokines and Microglial Activation
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Shin Jung-Won
Cheong Young-Jin
Koo Yong-Mo
Kim Soo-Yong
Noh Chung-Ku
Son Young-Ha
Kang Chul-Hun
Sohn Nak-Won
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Abstract
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α-Asarone exhibits a number of pharmacological actions including neuroprotective, anti-oxidative, anticonvulsive, and cognitive enhancing action. The present study investigated the effects of α-asarone on pro-inflammatory cytokines mRNA, microglial activation, and neuronal damage in the hippocampus and on learning and memory deficits in systemic lipopolysaccharide (LPS)-treated C57BL/6 mice. Varying doses of α-asarone was orally administered (7.5, 15, or 30 mg/kg) once a day for 3 days before the LPS (3 mg/kg) injection. α-Asarone significantly reduced TNF-α and IL-1β mRNA at 4 and 24 hours after the LPS injection at dose of 30 mg/kg. At 24 hours after the LPS injection, the loss of CA1 neurons, the increase of TUNEL-labeled cells, and the up-regulation of BACE1 expression in the hippocampus were attenuated by 30 mg/kg of α-asarone treatment. α-Asarone significantly reduced Iba1 protein expression in the hippocampal tissue at a dose of 30 mg/kg. α-Asarone did not reduce the number of Iba1-expressing microglia on immunohistochemistry but the average cell size and percentage areas of Iba1-expressing microglia in the hippocampus were significantly decreased by 30 mg/kg of α-asarone treatment. In the Morris water maze test, α-asarone significantly prolonged the swimming time spent in the target and peri-target zones. α-Asarone also significantly increased the number of target heading and memory score in the Morris water maze. The results suggest that inhibition of pro-inflammatory cytokines and microglial activation in the hippocampus by α-asarone may be one of the mechanisms for the α-asarone-mediated ameliorating effect on memory deficits.
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KEYWORD
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α-Asarone, Memory deficit, Microglial activation, TNF-α, IL-1β, Neuroinflammation
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