• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Drug Design, Development and Therapy >Botulinum Toxin Type A Possibly Affects Ca v 3.2 Calcium Channel Subunit in Rats with Spinal Cord Injury-Induced Muscle Spasticity
【24h】

Botulinum Toxin Type A Possibly Affects Ca v 3.2 Calcium Channel Subunit in Rats with Spinal Cord Injury-Induced Muscle Spasticity

机译：肉毒杆菌毒素类型A可能影响大鼠的Ca V 3.2钙通道亚基，脊髓损伤诱导的肌痉挛

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Introduction: Spinal cord injury (SCI) often causes muscle spasticity, which can be inhibited by using calcium channel blocker. Botulinum toxin type A (BoT-A) shows therapeutic efficacy on spasticity and may exert inhibitory effects on the calcium channel. Methods: A rat model with muscle spasticity was established after SCI via contusion and compression. Different concentrations (0, 1, 3 and 6 U/kg) of BoT-A Botox were injected in the extensor digitorum longus (EDL) muscles of the right hindlimb in the muscle spasticity model. The changes of muscle spasticity and calcium level in EDL muscles were measured after the establishment of SCI-induced spasticity. Cav 3.2 calcium channel subunit and its mutant (M1560V) were analyzed using Western blot before (input) or after immunoprecipitation with anti-FLAG antibody, and their currents were measured in motoneurons by using whole-cell voltage clamp recordings. Results: SCI induced muscle spasticity, whereas calcium level in EDL muscles and expression of Cav 3.2 was increased in the SCI model when compared with the sham group (p 0.05). BoT-A Botox treatment significantly reduced muscle spasticity and calcium level in EDL muscles and Cav 3.2 expression in a dose-dependent way (p 0.05). The ratio of biotinylated to total Cav 3.2 was reduced in the mutant (M1560V) of Cav 3.2 and lower than that in the wild Cav 3.2. BoT-A Botox intervention also reduced the current values of calcium channel and the ratio in a dose-dependent way (p 0.05). Discussion: BoT-A Botox possibly attenuates SCI-induced muscle spasticity by affecting the expression of Cav 3.2 calcium channel subunit in the rat models. There may be multiple mechanisms for the function of BoT-A Botox. Further work is needed to be done to address these issues.
机译：简介：脊髓损伤（SCI）通常会导致肌肉痉挛，这可以通过使用钙通道阻挡者来抑制。肉毒杆菌毒素类型A（BOT-A）显示了对痉挛性的治疗效果，并且可能对钙通道发挥抑制作用。方法：通过挫伤和压缩在SCI后建立了具有肌痉挛的大鼠模型。在肌肉痉挛模型的右后肢的伸肌位数（EDL）肌肉中注射不同浓度（0,1,3和6和6u / kg）的Bot-a botox。在建立SCI诱导的痉挛后测量EDL肌肉肌痉挛和钙水平的变化。使用蛋白质印迹或在用抗标志抗体的免疫沉淀之后分析CAV 3.2钙通道亚基及其突变体（M1560V），并通过使用全电池电压夹具记录在运动神经元中测量它们的电流。结果：SCI诱导肌痉挛，而与假组相比，SCI模型中EDL肌肉和CAV 3.2表达的钙水平增加（P <0.05）。 BOT-A Botox治疗在剂量依赖的方式中显着降低了EDL肌肉和CAV 3.2表达中的肌痉挛和钙水平（P <0.05）。在Cav 3.2的突变体（M1560V）中，生物素化至总腔3.2的比例降低，低于野生CAV 3.2中的突变体（M1560V）。 BOT-A BOTOX干预也降低了钙通道的电流值和以剂量依赖的方式（P <0.05）。讨论：BOT-A BOTOX可能通过影响大鼠模型中CAV 3.2钙通道亚基的表达来衰减SCI诱导的肌肉痉挛。可以存在多种机制的BOT-A Botox的功能。需要进一步的工作来解决这些问题。

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