背景:阿尔茨海默病(AD)的新诊断方法和疗法的发现面临重大挑战。先前的研究揭示了Apelin-13在神经退行性疾病中的神经保护特性。然而,阐明其对抗AD相关神经损伤的功效的潜在机制势在必行.在这项研究中,我们旨在研究Apelin-13在链脲佐菌素(STZ)诱导的AD体内模型中的作用机制。
方法:我们在小鼠中利用STZ诱导的AD神经损伤模型来研究Apelin-13给药的作用。Apelin-13鼻内给药,使用标准化行为测试评估认知障碍,主要是,行为评估,组织学分析,和生化化验,以评估突触可塑性和氧化应激信号通路。
结果:我们的发现表明,鼻内施用Apelin-13改善了STZ诱导的AD模型中的认知障碍。此外,我们观察到这种效应可能是由突触可塑性增强和氧化应激信号通路减弱所介导的.
结论:这项研究的结果表明,鼻内给药Apelin-13有望作为预防神经退行性疾病如AD的治疗策略。通过改善突触可塑性和减轻氧化应激,Apelin-13可能为AD和相关疾病的神经保护提供了一种新的方法。
BACKGROUND: The discovery of novel diagnostic methods and therapies for Alzheimer\'s disease (AD) faces significant challenges. Previous research has shed light on the neuroprotective properties of Apelin-13 in neurodegenerative disorders. However, elucidating the mechanism underlying its efficacy in combating AD-related nerve injury is imperative. In this study, we aimed to investigate Apelin-13\'s mechanism of action in an in vivo model of AD induced by streptozocin (STZ).
METHODS: We utilized an STZ-induced nerve injury model of AD in mice to investigate the effects of Apelin-13 administration. Apelin-13 was administered intranasally, and cognitive impairment was assessed using standardized behavioral tests, primarily, behavioral assessment, histological analysis, and biochemical assays, in order to evaluate synaptic plasticity and oxidative stress signaling pathways.
RESULTS: Our findings indicate that intranasal administration of Apelin-13 ameliorated cognitive impairment in the STZ-induced AD model. Furthermore, we observed that this effect was potentially mediated by the enhancement of synaptic plasticity and the attenuation of oxidative stress signaling pathways.
CONCLUSIONS: The results of this study suggest that intranasal administration of Apelin-13 holds promise as a therapeutic strategy for preventing neurodegenerative diseases such as AD. By improving synaptic plasticity and mitigating oxidative stress, Apelin-13 may offer a novel approach to neuroprotection in AD and related conditions.