We reported previously that geniposide showed neurotrophic and neuroprotective activities with the activation
of glucagons-like peptide 1 receptor (GLP-1R) in neurons. The current study was designed to further investigate the
protective effect of geniposide on β-amyloid (Aβ)-induced cytotoxicity. Our results showed that pre-incubation with
geniposide prevented Aβ1-42-induced cell injury in primary cultured cortical neurons. Geniposide also induced the
expression of insulin-degrading enzyme (IDE), a major degrading protease of Aβ, in a dose-dependent manner. Moreover,
bacitracin, an inhibitor of IDE, and RNAi on Glp-1r gene decreased the neuroprotection of geniposide in Aβ1-42-treated
cortical neurons. Our findings indicated that geniposide activating GLP-1R to against Aβ-induced neurotoxicity involved
in its regulation on the expression of IDE in cortical neurons, which provided an additional mechanistic insight into the
role of GLP-1R in neuroprotection.
Keywords: Alzheimer’s disease (AD), β-amyloid (Aβ), glucagon-like peptide 1 receptor (GLP-1R), insulin-degrading enzyme
(IDE), neuroprotection, neurotoxicity, cortical neurons, protease, endogenous, horseradish peroxidase.
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