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瓜蒌桂枝汤通过调节谷氨酸水平和 AMPA 受体表达发挥对脑卒中后痉挛的神经保护作用。

Gua Lou Gui Zhi decoction exerts neuroprotective effects on post-stroke spasticity via the modulation of glutamate levels and AMPA receptor expression.

机构信息

College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Minhou Shangjie, Fuzhou, Fujian 350108, PR China.

出版信息

Int J Mol Med. 2013 Apr;31(4):841-8. doi: 10.3892/ijmm.2013.1262. Epub 2013 Jan 30.

DOI:10.3892/ijmm.2013.1262
PMID:23443675
Abstract

Spasticity is one of the most physically debilitating disabilities following stroke and may slow down the potential success of rehabilitation. Glutamate and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors have been shown to play a crucial role in spasticity following cerebral ischemia/reperfusion (I/R) injury. Gua Lou Gui Zhi decoction (GLGZD) is a well-known traditional Chinese formula that has long been used clinically in China to treat muscular spasticity following stroke, epilepsy or spinal cord injury. However, the precise mechanisms behind its neuroprotective and anti-spasticity effects remain poorly understood. In the present study, using a rat model of focal cerebral I/R injury, we evaluated the neuroprotective and anti-spasticity effects of GLGZD and investigated the underlying mechanisms. We found that GLGZD improved neurological deficits and reduced infarct volumes in cerebral I/R-injured rats. In addition, GLGZD reduced cerebral ischemic spasticity since it improved the screen test and Hoffman's reflex (H-reflex) scores. It also reduced glutamate levels in the cerebrospinal fluid and altered the expression of the AMPA receptor subunits. Our data demonstrate that GLGZD exerts neuroprotective and anti-spasticity effects in a cerebral ischemia model via the modulation of glutamate levels and AMPA receptor expression.

摘要

痉挛是中风后最具身体致残性的障碍之一,可能会减缓康复的潜在成功。谷氨酸和α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)受体已被证明在脑缺血/再灌注(I / R)损伤后痉挛中发挥关键作用。瓜蒌桂枝汤(GLGZD)是一种著名的中药配方,在中国临床上长期用于治疗中风、癫痫或脊髓损伤后的肌肉痉挛。然而,其神经保护和抗痉挛作用的确切机制仍知之甚少。在本研究中,我们使用局灶性脑 I / R 损伤大鼠模型,评估了 GLGZD 的神经保护和抗痉挛作用,并探讨了其潜在机制。我们发现 GLGZD 改善了脑 I / R 损伤大鼠的神经功能缺损并减少了梗死体积。此外,GLGZD 降低了脑缺血性痉挛,因为它改善了屏幕测试和 Hoffman 反射(H-反射)评分。它还降低了脑脊液中的谷氨酸水平并改变了 AMPA 受体亚基的表达。我们的数据表明,GLGZD 通过调节谷氨酸水平和 AMPA 受体表达在脑缺血模型中发挥神经保护和抗痉挛作用。

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