Electroacupuncture Attenuates Cognitive Impairment in Rat Model of Chronic Cerebral Hypoperfusion via miR-137/NOX4 Axis

Abstract

Electroacupuncture has shown protective effects on cognitive decline. However, the underlying molecular mechanisms are not clear. The present study was conducted to determine whether the cognitive function was ameliorated in cerebral hypoperfusion rats following electroacupuncture and to investigate the role of miR-137/NOX4 axis. In this study, chronic cerebral hypoperfusion (CCH) model was established by bilateral common carotid artery occlusion. Electroacupuncture treatment attenuated brain injury in CCH model group via regulating miR-137/NOX4 axis. Furthermore, the data of neuronal apoptosis and oxidative stress were observed. Our findings indicated that (1) neuronal apoptosis and oxidative stress in CCH rats were significantly increased compared with control group; (2) the animal cognitive performance was evaluated using the Morris water maze (MWM). The results showed that electroacupuncture therapy ameliorated spatial learning and memory impairment in cerebral hypoperfusion rats; and (3) electroacupuncture therapy reduces neuronal apoptosis and oxidative stress by activating miR-137/NOX4 axis. These results suggest that electroacupuncture therapy for CCH may be mediated by miR-137/NOX4 axis. Electroacupuncture therapy may act as a potential therapeutic approach for chronic cerebral hypoperfusion.

Visualization and Analysis of the Mapping Knowledge Domain of Acupuncture and Central Nervous System Cell Apoptosis

“…The main points of the articles included in Evidence-Based Complementary and Alternative Medicine are as follows. Electroacupuncture therapy for CCH may be mediated by the miR-137/NOX4 axis [ 47 ]. The alleviation of inadequate autophagy and apoptosis may be a key mechanism involved in the reflex regulation of EA at GV26 to treat cerebral ischaemia [ 48 ].…”

Electroacupuncture of the Baihui and Shenting acupoints for vascular dementia in rats through the miR-81/IL-16/PSD-95 pathway

“…In rats with reduced brain perfusion, EA can inhibit neuronal apoptosis, improve learning disorders, and alleviate brain injury. Moreover, EA may also regulate the miR-137/NOX4 axis (10). The mechanism for increased LIM kinase-1 induced by EA may involve miR-134 located in the hippocampal CA1 region, where it enhances synapse-dendrite plasticity during the recovery phase of ischemic stroke through the negative regulation of LIM kinase-1 (11).…”