论文部分内容阅读
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.
Electroacupuncture (EA) has anti-oxidative and anti-inflammatory actions, but or 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 Unirrigated 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. EMC significantly reduced infarct volume, reduced 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, Nr f2 and glutamylcysteine synthetase (GCS) expression levels were markedly increased by EA. In transient, 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.