Electro-acupuncture potentiates the disulphide-reducing activities of thioredoxin system by increasing thioredoxin expression in ischemia-reperfused rat brains.
Electro-acupuncture potentiates the disulphide-reducing activities of thioredoxin system by increasing thioredoxin expression in ischemia-reperfused rat brains.
复制标题
DOI：
10.1016/j.lfs.2004.10.069
复制
发表时间：
2005-06
期刊：
影响因子：
6.1
通讯作者：
F. K. Siu;S. Lo;M. Leung
中科院分区：
文献类型：
--
作者：
F. K. Siu;S. Lo;M. Leung
活性氧可以通过硫醇部分的氧化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）可防止敏感蛋白质发生这种氧化修饰。氧化损伤是缺血中最具破坏性的应激之一。如果氧化应激能够最小化，所发生的损害也会相应地最小化。因此，我们研究了对缺血后大鼠的风池（GB20）或足三里（ST36）穴位进行电针（EA）治疗是否可以增加TR相关活性和Trx表达，从而维持周围易感蛋白的完整硫醇部分。我们的结果表明，任一穴位的电针治疗均可增加缺血再灌注脑组织中 Trx 的表达。诱导的Trx表达水平从缺血后第1天到第4天逐渐增加。统计分析显示，GB20和ST36时EA治疗的效果没有明显差异。假 EA 处理没有诱导任何 Trx 表达。任一穴位的电针均不会改变非缺血和缺血再灌注大鼠大脑中的 TR 活性。总的来说，我们的发现表明 GB20 或 ST36 的 EA 处理可以增加 Trx 表达，从而可以最大限度地减少周围蛋白质硫醇基团的氧化修饰。
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 electroacupuncture (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 any 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.