首页> 外文期刊>Mediators of inflammation >Auricular Electroacupuncture Reduced Inflammation-Related Epilepsy Accompanied by Altered TRPA1, pPKCα, pPKCε, and pERk1/2 Signaling Pathways in Kainic Acid-Treated Rats
【24h】

Auricular Electroacupuncture Reduced Inflammation-Related Epilepsy Accompanied by Altered TRPA1, pPKCα, pPKCε, and pERk1/2 Signaling Pathways in Kainic Acid-Treated Rats

机译:耳穴电针疗法减轻红藻酸治疗大鼠的炎症相关性癫痫伴TRPA1,pPKCα,pPKCε和pERk1 / 2信号通路的改变

获取原文
           

摘要

Background. Inflammation is often considered to play a crucial role in epilepsy by affecting iron status and metabolism. In this study, we investigated the curative effect of auricular acupuncture and somatic acupuncture on kainic acid- (KA-) induced epilepsy in rats.Methods. We established an epileptic seizure model in rats by KA (12 mg, ip). The 2 Hz electroacupuncture (EA) was applied at auricular and applied atZusanliandShangjuxu(ST36-ST37) acupoints for 20 min for 3 days/week for 6 weeks beginning on the day following the KA injection.Results. The electrophysiological results indicated that neuron overexcitation occurred in the KA-treated rats. This phenomenon could be reversed among either the auricular EA or ST36-ST37 EA treatment, but not in the sham-control rats. The Western blot results revealed that TRPA1, but not TRPV4, was upregulated by injecting KA and could be attenuated by administering auricular or ST36-ST37 EA, but not in the sham group. In addition, potentiation of TRPA1 was accompanied by increased PKCαand reduced PKCε. Furthermore, pERK1/2, which is indicated in inflammation, was also increased by KA. Furthermore, the aforementioned mechanisms could be reversed by administering auricular EA and could be partially reversed by ST36-ST37 EA.Conclusions. These results indicate a novel mechanism for treating inflammation-associated epilepsy and can be translated into clinical therapy.
机译:背景。人们通常认为炎症会通过影响铁的状态和代谢而在癫痫中起关键作用。在这项研究中,我们研究了耳针和体针疗法对海藻酸(KA-)诱发的癫痫大鼠的疗效。我们通过KA(12mg,ip)建立了大鼠癫痫发作模型。从KA注射后的第二天开始,在耳廓处应用2 Hz电针(EA),并在足三联商ju(ST36-ST37)穴位上应用20 min,连续3天/周,连续3周/天。电生理结果表明,在KA处理的大鼠中发生了神经元过度兴奋。在耳廓EA或ST36-ST37 EA治疗中,这种现象可以逆转,但在假对照大鼠中则不能。 Western印迹结果表明,通过注射KA可以上调TRPA1,而不是TRPV4,并且可以通过施用耳廓或ST36-ST37 EA来减弱,但在假手术组中则不能。另外,TRPA1的增强伴随着PKCα的增加和PKCε的减少。此外,KA还增加了炎症反应中所指示的pERK1 / 2。此外,上述机制可以通过服用耳廓EA逆转,也可以通过ST36-ST37 EA部分逆转。这些结果表明治疗炎症相关性癫痫的新机制,可以转化为临床治疗。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号