【摘 要】
：
Although glucagon-like peptide-1 (GLP-1), an insulin-releasing gut hormone, has been thought as a promising treatment for Alzhermers disease (AD), the natural GLP-1 can be rapidly degraded by the enzy
【机 构】
：
Department of Physiology,Key Laboratory of Cellular Physiology,Ministry of Education,Shanxi Medical
【出 处】
：
International Conference for Physiological Sciences 2012(201
论文部分内容阅读
Although glucagon-like peptide-1 (GLP-1), an insulin-releasing gut hormone, has been thought as a promising treatment for Alzhermers disease (AD), the natural GLP-1 can be rapidly degraded by the enzyme dipeptidyl peptidase Ⅳ (DPP Ⅳ).Lixisenatide, a novel long-lasting GLP-1 analogue, was found to be resistant to DPP Ⅳ and to have greater biological activity.However, there is not enough evidence for the neuroprotective effect of Lixisenatide in AD.The present study investigated the neuroprotective effect of Lixisenatide against Aβ25-35-induced neurotoxicity by using Morris water maze test and in vivo hippocampal field excitatory postsynaptic potential recording techniques.In behavioral tests, we found that: (1) Hippocampal injection of Amyloid β fragment 25-35 (Aβ25-35, 5 nmol) impaired the spatial learning and memory of rats;(2) Application of Lixisenatide alone did not affect cognitive behavior of rats, but effectively and dose-dependently protected spatial learning and memory of rats against Aβ25-35-induced impairment.In addition, the results from electrophysiological experiments showed that:(1) Aβ25-35 significantly suppressed hippocampal long term potentiation (LTP) of fEPSPs.(2) Lixisenatide alone did not affect LTP, but effectively prevented Aβ25-35-induced suppression of LTR The present study, therefore, provides a behavioral and an electrophysiological evidence for the neuroprotective effects of Lixisenatide and suggests a potential clinical value of Lixisenatide in the prevention and treatment of AD in the future.
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