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Electro-acupuncture potentiates the disulphide-reducing activities of thioredoxin system by increasing thioredoxin expression in ischemia-reperfused rat brains

机译:电针通过增加缺血再灌注大鼠脑中的硫氧还蛋白表达来增强硫氧还蛋白系统的二硫化物还原活性

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摘要

Reactive oxygen species can directly affect the conformation and activity of sulfhydryl-containing proteins by oxidation of their thiol moiety. During the process of ischemia-reperfusion, the thioredoxin (Trx) system (consisting of thioredoxin reductase (TR), Trx and NADPH) prevents susceptible proteins from this oxidative modification. Oxidative damage is one of the most damaging stress in ischemia. If oxidative stress could be minimized, the damage occurred will be minimized accordingly. We therefore investigated whether electro-acupuncture (EA) treatment at Fengchi (GB20) or Zusanli (ST36) acupoints in post-ischemic rats could increase TR-related activities and Trx expression which Would translate into maintaining the intact thiol moiety of susceptible proteins in the surrounding. Our results indicated that EA treatment at either acupoint increased the Trx expression in ischemic-reperfused brain tissues. Induced Trx expressed levels gradually increased from post-ischemia day 1 to day 4. Statistical analysis revealed that there was no observable difference in the effect of EA treatment at GB20 and ST36. Sham EA treatment did not induce my Trx expression, EA at either acupoint did not alter TR activities in both non-ischemic and ischemic-reperfused rat brains, Taken overall, our finding Suggests that EA treatment at GB20 or ST36 could increase Trx expression which could minimize oxidative modifications of thiol groups of surrounding proteins. (c) 2005 Elsevier Inc. All rights reserved.
机译:活性氧可以通过氧化巯基部分直接影响含巯基蛋白质的构象和活性。在缺血再灌注过程中,硫氧还蛋白(Trx)系统(由硫氧还蛋白还原酶(TR),Trx和NADPH组成)可防止易感蛋白质发生这种氧化修饰。氧化损伤是缺血中最具破坏力的压力之一。如果可以使氧化应激最小化,则相应地将发生的损害最小化。因此,我们研究了缺血后大鼠中风池(GB20)或足三里(ST36)穴位的电针(EA)处理是否可以增加TR相关活性和Trx表达,从而转化为维持易感蛋白质中完整的巯基部分。周围。我们的结果表明,在任一穴位进行EA治疗均可增加缺血再灌注脑组织中的Trx表达。从缺血后第1天到第4天,诱导的Trx表达水平逐渐增加。统计分析表明,在GB20和ST36时,EA治疗的效果没有明显差异。 Sham EA治疗未诱导我的Trx表达,非穴位和缺血再灌注大鼠脑中任一穴位的EA均未改变TR活性,总的来说,我们的发现表明,GB20或ST36 EA治疗可增加Trx表达,这可能尽量减少周围蛋白质的巯基的氧化修饰。 (c)2005 Elsevier Inc.保留所有权利。

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