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电针通过TrkA通路对大鼠脑缺血/再灌注后TRPM7 mRNA表达的影响。

Effect of electroacupuncture on TRPM7 mRNA expression after cerebral ischemia/reperfusion in rats via TrkA pathway.

作者信息

Zhao Li, Shi Jing, Sun Ning, Tian Shunlian, Meng Xianfang, Liu Xiaochun, Li Lingli

机构信息

Department of Neurobiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.

出版信息

J Huazhong Univ Sci Technolog Med Sci. 2005;25(3):247-50. doi: 10.1007/BF02828132.

Abstract

The effect of electroacupuncture (EA) on TRPM7 mRNA expression of focal cerebral ischemia in rats and further the role of EA in the relationship between TRPM7 and trkA pathway was investigated. Thirty SD rats were randomly divided into 5 groups : normal group, ischemia/reperfusion group, EA treated group (ischemic rats with EA treatment), TE infusion group (ischemic rats with EA treatment and TE buffer infusion), AS-ODN group (ischemic rats with EA treatment and antisense trkA oligonucleotide infusion). The stroke animal model was established by the modified method of middle cerebral artery occlusion. Antisense trkA oligonucleotide that blocked NGFs effects was injected into cerebroventricle before EA. The TRPM7 mRNA was detected by RT-PCR method. The results showed that there were low TRPM7 mRNA levels in cortex and hippocampus in normal group. Compared with normal group, TRPM7 mRNA expression was increased significantly in ischemia/reperfusion group (P<0.05). A significant reduction in the expression of TR-PM7 mRNA was found in EA treated group in contrast to ischemia/reperfusion group (P<0.05). The expression of TRPM7 mRNA in AS-ODN group was remarkably increased compared with EA treated group and TE infusion group (P<0.05). The results indicated that TRPM7 channels in the ischemic cortex and hippocampus in rats might play a key role in ischemic brain injury. EA could reverse the overexpression of TRPM7 in cerebral ischemia/reperfusion rats. And the inhibitory effect of EA on TRPM7 channels might be through trkA pathway.

摘要

研究了电针(EA)对大鼠局灶性脑缺血TRPM7 mRNA表达的影响,以及EA在TRPM7与trkA通路关系中的作用。将30只SD大鼠随机分为5组:正常组、缺血/再灌注组、电针治疗组(缺血大鼠接受电针治疗)、TE灌注组(缺血大鼠接受电针治疗并灌注TE缓冲液)、AS-ODN组(缺血大鼠接受电针治疗并灌注反义trkA寡核苷酸)。采用改良的大脑中动脉闭塞法建立脑卒中动物模型。在电针治疗前向脑室注射阻断NGF作用的反义trkA寡核苷酸。采用RT-PCR法检测TRPM7 mRNA。结果显示,正常组皮质和海马中TRPM7 mRNA水平较低。与正常组相比,缺血/再灌注组TRPM7 mRNA表达显著增加(P<0.05)。与缺血/再灌注组相比,电针治疗组TR-PM7 mRNA表达显著降低(P<0.05)。与电针治疗组和TE灌注组相比,AS-ODN组TRPM7 mRNA表达显著增加(P<0.05)。结果表明,大鼠缺血皮质和海马中的TRPM7通道可能在缺血性脑损伤中起关键作用。电针可逆转脑缺血/再灌注大鼠TRPM7的过度表达。电针抑制TRPM7通道的作用可能是通过trkA通路实现的。

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