The Institute of Rehabilitation Industry, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, 350122, China.
National-Local Joint Engineering Research Center of Rehabilitation Medicine Technology, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, 350122, China.
Biol Res. 2023 Jun 30;56(1):36. doi: 10.1186/s40659-023-00448-z.
Electroacupuncture (EA) is a complementary and alternative therapy which has shown protective effects on vascular cognitive impairment (VCI). However, the underlying mechanisms are not entirely understood.
Rat models of VCI were established with cerebral ischemia using occlusion of the middle cerebral artery or bilateral common carotid artery. The brain structure and function imaging were measured through animal MRI. miRNA expression was detected by chip and qPCR. Synaptic functional plasticity was detected using electrophysiological techniques.
This study demonstrated the enhancement of Regional Homogeneity (ReHo) activity of blood oxygen level-dependent (BOLD) signal in the entorhinal cortical (EC) and hippocampus (HIP) in response to EA treatment. miR-219a was selected and confirmed to be elevated in HIP and EC in VCI but decreased after EA. N-methyl-D-aspartic acid receptor1 (NMDAR1) was identified as the target gene of miR-219a. miR-219a regulated NMDAR-mediated autaptic currents, spontaneous excitatory postsynaptic currents (sEPSC), and long-term potentiation (LTP) of the EC-HIP CA1 circuit influencing synaptic plasticity. EA was able to inhibit miR-219a, enhancing synaptic plasticity of the EC-HIP CA1 circuit and increasing expression of NMDAR1 while promoting the phosphorylation of downstream calcium/calmodulin-dependent protein kinase II (CaMKII), improving overall learning and memory in VCI rat models.
Inhibition of miR-219a ameliorates VCI by regulating NMDAR-mediated synaptic plasticity in animal models of cerebral ischemia.
电针（EA）是一种补充和替代疗法，已显示对血管性认知障碍（VCI）具有保护作用。然而，其潜在机制尚不完全清楚。
通过大脑中动脉或双侧颈总动脉闭塞建立 VCI 大鼠模型。通过动物 MRI 测量脑结构和功能成像。通过芯片和 qPCR 检测 miRNA 表达。通过电生理技术检测突触功能可塑性。
本研究证明了电针对大脑中动脉或双侧颈总动脉闭塞导致的 VCI 大鼠模型的海马（HIP）和内嗅皮层（EC）脑区血氧水平依赖（BOLD）信号的区域同质性（ReHo）活动增强。选择并证实 miR-219a 在 HIP 和 EC 中升高，但电针后降低。N-甲基-D-天冬氨酸受体 1（NMDAR1）被确定为 miR-219a 的靶基因。miR-219a 调节 NMDAR 介导的自突触电流、自发性兴奋性突触后电流（sEPSC）和 EC-HIP CA1 回路的长时程增强（LTP），影响突触可塑性。电针能够抑制 miR-219a，增强 EC-HIP CA1 回路的突触可塑性，增加 NMDAR1 的表达，同时促进下游钙/钙调蛋白依赖性蛋白激酶 II（CaMKII）的磷酸化，改善 VCI 大鼠模型的整体学习和记忆。
在缺血性脑动物模型中，抑制 miR-219a 通过调节 NMDAR 介导的突触可塑性来改善 VCI。
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