【摘 要】
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Recently,it has been demonstrated that TRPM7 is an essential mediator of anoxia-induced neuronal death which is activated by oxidative stress.Meanwhile,nerv
【机 构】
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Department of Neurobiology, Tongii Medical College, Huazhong Science and Technology University, Wuha
【出 处】
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中国神经科学学会第四次会员代表大会暨第七届全国学术会议(The 7th Biennial Meeting and the
论文部分内容阅读
Recently,it has been demonstrated that TRPM7 is an essential mediator of anoxia-induced neuronal death which is activated by oxidative stress.Meanwhile,nerve growth factor (NGF) is known to have survival and neuroprotective effects by interacting with a specific tyrosine kinase receptor,trkA.In the present study,we found that electroacupuncture (EA) treatment could up-regulate trkA expression of focal cerebral ischemia in rats.At the same time,EA therapy remarkably decreased the high expression of TRPM7 induced by ischemia.Using K252a to inhibit trkA,we found that the EA-mediated down-regulation of TRPM7 was significantly suppressed in cerebral ischemia rats.TrkA can utilize two distinct signalling pathways:phosphatidylinositol 3-kinase (PI3K) pathway and extracellular signal-related kinase (ERK) pathway.We found that the effect of EA treatment on TRPM7 was also inhibited by PI3K inhibitor,while ERK inhibitor had no effect.Taken overall,our findings suggest that EA could reverse the ischemia-induced increase of TRPM7 level,mainly through the activation of trkA,which could be linked to PI3K.
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