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Electroacupuncture Alleviated Neuronal Apoptosis Following Ischemic Stroke in Rats via Midkine and ERK/JNK/p38 Signaling Pathway. | LitMetric

Electroacupuncture Alleviated Neuronal Apoptosis Following Ischemic Stroke in Rats via Midkine and ERK/JNK/p38 Signaling Pathway.

J Mol Neurosci

Department of Rehabilitation Medicine, The Third Hospital of Hebei Medical University, No. 139 Ziqiang Road, Shijiazhuang, 050051, Hebei, People's Republic of China.

Published: September 2018

AI Article Synopsis

  • This study investigated the effects of electroacupuncture (EA) on rats that experienced middle cerebral artery occlusion (MCAO) and subsequent reperfusion, focusing on parameters of brain health.
  • Fifty-four male Sprague-Dawley rats were divided into three groups: a sham group, an MCAO/R group, and an EA-treated group, with EA applied at specific acupoints for three consecutive days.
  • The results showed that EA treatment reduced brain damage, improved neurological function, decreased apoptotic cells, and upregulated a growth factor (midkine), suggesting that EA may protect neuronal health by impacting specific signaling pathways related to stress responses.

Article Abstract

This study aimed to evaluate the effects of electroacupuncture (EA) intervention administered at rats of middle cerebral artery occlusion (MCAO)/reperfusion. Fifty-four male Sprague-Dawley rats were divided into three groups, consisting of sham group, MCAO/R group, and EA group. EA treatment at Quchi and Zusanli acupoints was applied in rats of EA group at 24 h after MCAO once per day for 3 days. Our results indicated that EA treatment reduced infarct volumes and neurological deficits, as well alleviated the apoptotic cells in peri-infarct cortex, indicating that EA exerted neuroprotective effect in cerebral ischemic rats. Moreover, EA treatment may effectively reverse the upregulation of caspase-3 and Bim and alleviate the inhibition of Bcl-2 following 72-h ischemic stroke. EA may significantly reverse the promoted relative density level of p-ERK1/2, p-JNK, and p-p38 in the EA group compared with the MCAO/R group. In addition, the growth factor midkine (MK) was upregulated at 72 h after MCAO/R, and EA treatment may significantly prompt expression of MK. Our study demonstrated that EA exerted neuroprotective effect against neuronal apoptosis and the mechanism might involve in upregulation of MK and mediation of ERK/JNK/p38 signal pathway.

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Source
http://dx.doi.org/10.1007/s12031-018-1142-yDOI Listing

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