4.4 Article

Electroacupuncture stimulates the proliferation and differentiation of endogenous neural stem cells in a rat model of ischemic stroke

期刊

EXPERIMENTAL AND THERAPEUTIC MEDICINE
卷 16, 期 6, 页码 4943-4950

出版社

SPANDIDOS PUBL LTD
DOI: 10.3892/etm.2018.6848

关键词

neural stem cells; electroacupuncture; plasticity-related gene 5; RhoA; cerebral ischemia

资金

  1. National Natural Science of Foundation of China [81072947, 81473470]
  2. Guangdong Natural Science Foundation [8152800007000001, 2014A030311033]

向作者/读者索取更多资源

Electroacupuncture (EA) may stimulate neurogenesis in animal models of ischemic stroke; however, the associated mechanisms are not clear. The present study aimed to evaluate the neurogenesis efficacy of EA on ischemic stroke and the underlying associated mechanisms. A model of middle cerebral artery occlusion (MCAO) was employed as the rat model of brain ischemia and reperfusion. EA treatment at the GV20 (Baihui) and GV14 (Dazhui) acupoints was conducted for 30 min daily following MCAO. Immunofluorescence was performed to measure the number of bromodeoxyuridine (BrdU)/nestin- or BrdU/doublecortin (DCX)-positive cells in the sham, MCAO and MCAO + EA groups. Results indicated that EA stimulation significantly decreased the neurological score and neuronal loss in rats in the MCAO group (both P<0.05). Furthermore, immunostaining assays indicated that BrdU/nestin- and BrdU/DCX-positive cells in EA-treated rats were significantly increased (P<0.05) when compared with the rats in the MCAO group, indicating EA may induce the proliferation and differentiation of endogenous neural stem cells (eNSCs) during cerebral ischemia-reperfusion. In addition, EA treatment significantly enhanced the protein expression levels of plasticity-related gene 5 (PRG5), a critical neurogenesis factor, and significantly decreased the protein expression levels of three neurogenesis inhibiting molecules, NogoA, lysophosphatidic acid and RhoA (all P<0.05). These results suggested that EA promotes the proliferation and differentiation of eNSCs, likely through modulating PRG5/RhoA signaling.

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