Electroacupuncture（EA） has anti-oxidative and anti-inflammatory actions,but whether the neuroprotective effect of EA against cerebral ischemia-reperfusion（I/R） injury involves modulation of the extracellular regul...Electroacupuncture（EA） has anti-oxidative and anti-inflammatory actions,but whether the neuroprotective effect of EA against cerebral ischemia-reperfusion（I/R） injury involves modulation of the extracellular regulated kinase 1/2（ERK1/2） signaling pathway is unclear.Middle cerebral artery occlusion（MCAO） was performed in Sprague-Dawley rats for 2 hours followed by reperfusion for 24 hours.A 30-minute period of EA stimulation was applied to both Baihui（DU20） and Dazhui（DU14） acupoints in each rat（10 mm EA penetration depth,continuous wave with a frequency of 3 Hz,and a current intensity of 1–3 m A） when reperfusion was initiated.EA significantly reduced infarct volume,alleviated neuronal injury,and improved neurological function in rats with MCAO.Furthermore,high m RNA expression of Bax and low m RNA expression of Bcl-2 induced by MCAO was prevented by EA.EA substantially restored total glutathione reductase（GR）,glutathione（GSH） and glutathione peroxidase（GSH-Px） levels.Additionally,Nrf2 and glutamylcysteine synthetase（GCS） expression levels were markedly increased by EA.Interestingly,the neuroprotective effects of EA were attenuated when ERK1/2 activity was blocked by PD98059（a specific MEK inhibitor）.Collectively,our findings indicate that activation of the ERK1/2 signaling pathway contributes to the neuroprotective effects of EA.Our study provides a better understanding of the regulatory mechanisms underlying the therapeutic effectiveness of EA.展开更多
基金supported by the National Natural Science Foundation of China,No.81373748,81171659,11574156 and 81403136a grant from the 333 Project of Jiangsu Province in China No.BRA2014341a grant from the Jiangsu Province Science and Technology Support Project in China,No.BE2010769
文摘Electroacupuncture（EA） has anti-oxidative and anti-inflammatory actions,but whether the neuroprotective effect of EA against cerebral ischemia-reperfusion（I/R） injury involves modulation of the extracellular regulated kinase 1/2（ERK1/2） signaling pathway is unclear.Middle cerebral artery occlusion（MCAO） was performed in Sprague-Dawley rats for 2 hours followed by reperfusion for 24 hours.A 30-minute period of EA stimulation was applied to both Baihui（DU20） and Dazhui（DU14） acupoints in each rat（10 mm EA penetration depth,continuous wave with a frequency of 3 Hz,and a current intensity of 1–3 m A） when reperfusion was initiated.EA significantly reduced infarct volume,alleviated neuronal injury,and improved neurological function in rats with MCAO.Furthermore,high m RNA expression of Bax and low m RNA expression of Bcl-2 induced by MCAO was prevented by EA.EA substantially restored total glutathione reductase（GR）,glutathione（GSH） and glutathione peroxidase（GSH-Px） levels.Additionally,Nrf2 and glutamylcysteine synthetase（GCS） expression levels were markedly increased by EA.Interestingly,the neuroprotective effects of EA were attenuated when ERK1/2 activity was blocked by PD98059（a specific MEK inhibitor）.Collectively,our findings indicate that activation of the ERK1/2 signaling pathway contributes to the neuroprotective effects of EA.Our study provides a better understanding of the regulatory mechanisms underlying the therapeutic effectiveness of EA.
