| 30552029 |
Electroacupuncture Regulates Hippocampal Synaptic Plasticity via Inhibiting Janus-Activated Kinase 2/Signal Transducer and Activator of Transcription 3 Signaling in Cerebral Ischemic Rats. |
J Stroke Cerebrovasc Dis. 2019 Mar;28(3):792-799. doi: 10.1016/j.jstrokecerebrovasdis.2018.11.025. Epub 2018 Dec 12. |
2019 Mar |
OBJECTIVE: To determine the mechanism(s) involved in electroacupuncture (EA)-mediated improvements in synaptic plasticity in a rat model of middle cerebral artery occlusion and reperfusion (MCAO/R)-induced cognitive deficits. METHODS: Focal cerebral ischemic stroke was induced by (MCAO/R) surgery. Rats were randomly split into 4 groups: control group (sham operation control), MCAO group, Baihui (GV 20) and Shenting (GV 24) acupoint EA group (verum acupuncture, MCAO鈥?鈥疺A), and nonacupoint EA group (control acupuncture, MCAO鈥?鈥疌A). EA treatment was administered for 14 consecutive days in MCAO鈥?鈥疺A and MCAO鈥?鈥疌A groups. Neurological assessment, behavioral performance testing, and molecular biology assays were used to evaluate the MCAO/R model, EA therapeutic effect and potential therapeutic mechanism(s) of EA. RESULTS: Significant amelioration of neurological deficits was found in MCAO鈥?鈥疺A rats compared with MCAO rats (P < .01). Moreover, learning and memory significantly improved in EA-treated rats compared with MCAO or MCAO鈥?鈥疌A rats (P < .05) together with an increase in the number of PSD-95(+) and SYN(+) cells and synapses in the hippocampal CA1 region (P < .05). MCAO鈥?鈥疺A rats also showed amelioration of pathological synaptic ultrastructural changes compared with MCAO or MCAO鈥?鈥疌A groups (P < .001). In contrast, EA decreased the levels and phosphorylation of JAK2 (Janus-activated kinase 2) and STAT3 (signal transducer and activator of transcription 3) in the hippocampal CA1 region compared with MCAO or MCAO鈥?鈥疌A group (P < .01). CONCLUSION: EA at GV 20 and GV 24 acupoints improved cognitive deficits in cerebral ischemic rats via the JAK2/STAT3 signaling pathway and mediated synaptic plasticity in the peri-infarct hippocampal CA1 region of rats following ischemic stroke."
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