Key result
Electroacupuncture reduces infarct volume and neurological deficits in stroke models via miR-9 upregulation.
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The aim of the present study was to investigate the neuroprotective mechanism of the miR-9-mediated activation of the nuclear factor (NF)-κB signaling pathway by electroacupuncture (EA) stimulation of the Quchi (LI11) and Zusanli (ST36) acupoints in a rat model of middle cerebral artery occlusion (MCAO). The present study demonstrated that EA alleviated the symptoms of neurological deficits and reduced the infarct volume in the rat brains. The expression of miR-9 in the peri-infarct cortex was increased in the EA group compared with the MCAO group, and the expression of NF-κB signaling pathway-associated factors, NF-κB p65, tumor necrosis factor (TNF)-α and interleukin (IL)-1β were reduced. Notably, miR-9 inhibitors were revealed to have the ability to suppress EA-alleviated cerebral inflammation and the expression of NF-κB downstream-related factors, NF-κB p65, TNF-α and IL-1β, and caused no alteration on the level of NF-κB upstream-related protein inhibitor of κBα, suggesting that the cerebral protective efficacy of EA targets miR-9-mediated NF-κB downstream pathway following ischemic stroke.
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Liu et al. (2015) studied Ischemic stroke (middle cerebral artery occlusion rat model). Electroacupuncture stimulation at Quchi (LI11) and Zusanli (ST36) acupoints vs. Middle cerebral artery occlusion (MCAO) control and miR-9 inhibitors was evaluated on Neurological deficits, cerebral infarct volume, and expression of miR-9 and NF-κB signaling pathway factors (NF-κB p65, TNF-α, IL-1β). Electroacupuncture at LI11 and ST36 alleviated neurological deficits and infarct volume in MCAO rats by upregulating miR-9 and inhibiting downstream NF-κB p65, TNF-α, and IL-1β.
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