KMID : 0043320170400050571
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Archives of Pharmacal Research 2017 Volume.40 No. 5 p.571 ~ p.578
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Geniposide attenuates the level of A¥â1?42 via enhancing leptin signaling in cellular and APP/PS1 transgenic mice
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Liu Zi Xuan
Zhang Yong Lan Liu Jian Hui Yin Fei
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Abstract
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An large body of evidence indicates that leptin has protective role against Alzheimer¡¯s disease, where it reduces ¥â-amyloid (A¥â) production in both cell culture and animal models. Our previous studies revealed that geniposide could attenuate the production of A¥â1?42 and antagonize the neurotoxicity of A¥â1?42 in neurons. However, the mechanism that underlies these effects remains to be clarified. To investigate whether leptin signaling is involved in regulating the production of A¥â1?42 by geniposide, we treated primary neurons with leptin antagonist (LA), and determined the influence of LA on the activities of leptin signaling molecules and the expressions of secretases associated with the production of A¥â1?42. The finding showed that, accompanied with the inhibition on the level of A¥â1?42 in primary neurons and APP/PS1 transgenic mice, geniposide induced the phosphorylation of JAK2 and STAT3, regulated the expression level of ¥á- and ¥â-secretase, and all of these could be prevented by the pre-incubation with LA. The results of this study suggest that geniposide may regulate the production of A¥â1?42 via leptin signaling.
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KEYWORD
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¥â-Amyloid (A¥â), AMP-activated protein kinase (AMPK), Geniposide, Leptin signaling, Leptin antagonist (LA)
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