Electroacupuncture promotes oligodendrocyte differentiation and myelin repair in a rat model of vascular dementia: Investigation of the mechanism from NF-κB-mediated inflammation

Abstract

Myelin impairment is an important cause of cognitive impairment in vascular dementia (VD). Promoting myelin regeneration has become an important improvement strategy and oligodendrocytes are important targets. This study used a multiple microinfarctions (MMI)-induced VD rat model to reveal the mechanism of myelination of oligodendrocytes in the recovery of VD model, and to investigate the intervention mechanism of electroacupuncture (EA), an effective therapeutic for VD. Initially, our transcriptomic analysis identified 52 differentially expressed genes between the sham and MMI groups. These genes are primarily associated with axonal pathways, including the synaptic vesicle cycle, glutamatergic synapse, axon guidance, and sphingolipid metabolism. Compared with sham group, inflammation, impaired differentiation of oligodendrocyte precursor cells (OPCs) and myelin damage were remarkably observable in the hippocampus of MMI group, indicating the involvement of inflammation-regulated impairment of OPCs. Accordingly, pyrrolidinedithiocarbamate (PDTC), a NF-κB inhibitor could improve learning and memory impairment, reverse the hippocampal inflammation and impairment of OPCs differentiation, and decrease myelin damage in MMI rats. Importantly, EA could also improve learning and memory, attenuate the inflammatory response in the hippocampus and facilitate the differentiation of OPCs to aid in the repair of myelin damage in MMI rats. In conclusion, our data suggest that NF-κB activation is a prohibited factor for the myelin repair, while EA might reduce NF-κB activation and promote the differentiation of OPCs to repair the myelin damage in MMI rats.