Basir Hamid Shokati, Mirazi Naser, Komaki Alireza, Hosseini Abdolkarim
Department of Biology, Faculty of Basic Science, Bu-Ali Sina University, Hamedan, Iran.
Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
Front Pharmacol. 2024 May 2;15:1379264. doi: 10.3389/fphar.2024.1379264. eCollection 2024.
Alzheimer's disease (AD) causes progressive loss of cognitive function and synaptic plasticity, which is the most common form of dementia. The present study was designed to scrutinize the effects of cacao on passive avoidance memory function and to identify the roles of hippocampal synaptic plasticity and oxidative stress in an AD rat model induced by unilateral intracerebroventricular (UICV) injection of amyloid-beta (Aβ). Oral administration of cacao (500 mg/kg/ day) was given for 2 consecutive months. A memory retention test was conducted 24 h after passive avoidance training was completed. Subsequently, the amplitude of population spike (PS) and slope of field excitatory postsynaptic potentials (fEPSPs) were assessed at hippocampal long-term potentiation (LTP) in perforant pathway-dentate gyrus (PP-DG) synapses. Moreover, total thiol group (TTG) and malondialdehyde (MDA) concentrations were evaluated in the plasma. Furthermore, compact Aβ plaques were detected in the hippocampal DG by performing Congo red staining. As a result of AD induction, passive avoidance memory was impaired; also, reduced fEPSP slopes, PS amplitudes, and content of TTG, and increase in MDA levels in the rats were observed. In contrast, cacao treatment ameliorated passive avoidance memory impairment, improved hippocampal LTP impairment, modulated oxidative-antioxidative status, and delayed Aβ plaques production in AD rats. Conclusively, cacao alleviates Aβ-induced cognitive deficit, probably by the amelioration of hippocampal LTP impairment, modulation of oxidative-antioxidative status, and inhibition of Aβ plaque accumulation.
阿尔茨海默病（AD）会导致认知功能和突触可塑性的渐进性丧失，它是痴呆最常见的形式。本研究旨在仔细研究可可对被动回避记忆功能的影响，并确定海马突触可塑性和氧化应激在单侧脑室内（UICV）注射β-淀粉样蛋白（Aβ）诱导的AD大鼠模型中的作用。连续2个月每天口服给予可可（500毫克/千克）。在被动回避训练完成24小时后进行记忆保持测试。随后，在穿通通路-齿状回（PP-DG）突触的海马长时程增强（LTP）处评估群体峰电位（PS）的幅度和场兴奋性突触后电位（fEPSP）的斜率。此外，还评估了血浆中的总硫醇基团（TTG）和丙二醛（MDA）浓度。此外，通过刚果红染色在海马齿状回中检测到致密的Aβ斑块。由于AD诱导，被动回避记忆受损；此外，还观察到大鼠的fEPSP斜率、PS幅度和TTG含量降低，以及MDA水平升高。相比之下，可可治疗改善了AD大鼠的被动回避记忆损伤，改善了海马LTP损伤，调节了氧化-抗氧化状态，并延缓了Aβ斑块的产生。总之，可可可能通过改善海马LTP损伤、调节氧化-抗氧化状态和抑制Aβ斑块积累来减轻Aβ诱导的认知缺陷。
