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1.
Acta Physiologica Sinica ; (6): 265-275, 2016.
Artículo en Chino | WPRIM | ID: wpr-331657

RESUMEN

The accumulation and neurotoxicity of amyloid β protein (Aβ) in the brain is one of major pathological hallmarks of Alzheimer's disease (AD). The effective drugs against Aβ have been still deficient up to now. According to a most recent study, (D-Ser2) Oxm, a new antidiabetic drug, not only improves the disorders in plasma glucose and insulin in type 2 diabetes mellitus (T2DM) rats, but also exerts positive effects on hippocampal neurogenesis and synaptogenesis. However, it is still unclear whether (D-Ser2)Oxm can directly protect cultured neurons against Aβ1-42-induced cytotoxicity. In the present study, we investigated the neuroprotective effects of (D-Ser2)Oxm on the cultured primary hippocampal neurons by testing the cell viability, neuronal apoptosis, mitochondrial membrane potential and intracellular calcium concentration. The results showed that treatment with (D-Ser2)Oxm effectively reversed Aβ1-42-induced decline in cell viability (P < 0.001), and this protective effect could be inhibited by the pretreatment with exendin(9-39), a GLP-1 receptor blocker. (D-Ser2)Oxm treatment also decreased Aβ1-42-induced neuronal early apoptosis and down-regulated apoptotic protein caspase3. Meantime, (D-Ser2)Oxm treatment inhibited Aβ1-42-induced [Ca(2+)]i elevation, mitochondrial membrane potential depolarization, and glycogen synthase kinase-3β (GSK3β) activation. These results suggest that (D-Ser2)Oxm can protect hippocampal neurons against Aβ1-42-induced cytotoxicity and this effect may be related to activation of GLP-1 receptors, regulation of intracellular calcium homeostasis and stabilization of mitochondrial membrane potential.


Asunto(s)
Animales , Ratas , Péptidos beta-Amiloides , Calcio , Supervivencia Celular , Diabetes Mellitus Tipo 2 , Receptor del Péptido 1 Similar al Glucagón , Hipocampo , Hipoglucemiantes , Insulina , Potencial de la Membrana Mitocondrial , Neurogénesis , Neuronas , Fármacos Neuroprotectores
2.
Chinese Journal of Applied Physiology ; (6): 18-21, 2016.
Artículo en Chino | WPRIM | ID: wpr-254966

RESUMEN

<p><b>OBJECTIVE</b>The present study investigated the effects of rapamycin on Aβ1-42-induced deficits in working memory and synaptic plasticity.</p><p><b>METHODS</b>After bilateral hippocampal injection of Aβ1-42 and rapamycinin rats, spontaneous alternation in Y-maze and in vivo hippocampal long-term potentiation (LTP) of rats were recorded. All data were analized by two-way repeated measures analysis of variance (ANOVA).</p><p><b>RESULTS</b>(Hippocampal injection of Aβ1-42 alone impaired working memory of rats; (2) Rapamycin did not affect working memory of rats, but alleviated Aβ1-42-induced working memory deficits, compared with Aβ1-42 alone group; (Aβ1-42 remarkably suppressed in vivo hippocampal LTP of fEPSPs in the CA1 region; (4) Pretreatment with rapamycin prevented Aβ1-42-induced suppression of LTP.</p><p><b>CONCLUSION</b>These data indicates that rapamycin could protect against Aβ1-42-induced impairments in working memory and synaptic plasticity in rats.</p>


Asunto(s)
Animales , Ratas , Péptidos beta-Amiloides , Hipocampo , Potenciación a Largo Plazo , Aprendizaje por Laberinto , Memoria a Corto Plazo , Plasticidad Neuronal , Fragmentos de Péptidos , Sirolimus , Farmacología
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