Department of Neurochemistry, Beijing Neurosurgical Institute, 6 Tiantan Xili, Chongwen District, Beijing, China.
Amino Acids. 2011 May;40(5):1419-29. doi: 10.1007/s00726-010-0751-8. Epub 2010 Sep 23.
Taurine, an abundant amino acid in the nervous system, is reported to reduce ischemic brain injury in a dose-dependent manner. This study was designed to investigate whether taurine protected brain against experimental stroke through affecting mitochondria-mediated cell death pathway. Rats were subjected to 2-h ischemia by intraluminal filament, and then reperfused for 22 h. It was confirmed again that taurine (50 mg/kg) administered intravenously 1 h after ischemia markedly improved neurological function and decreased infarct volume at 22 h after reperfusion. In vehicle-treated rats, the levels of intracellular ATP and the levels of cytosolic and mitochondrial Bcl-xL in the penumbra and core were markedly reduced, while the levels of cytosolic Bax in the core and mitochondrial Bax in the penumbra and core were enhanced significantly. There was a decrease in cytochrome C in mitochondria and an increase in cytochrome C in the cytosol of the penumbra and core. These changes were reversed by taurine. Furthermore, taurine inhibited the activation of calpain and caspase-3, reduced the degradation of αII-spectrin, and attenuated the necrotic and apoptotic cell death in the penumbra and core. These data demonstrated that preserving the mitochondrial function and blocking the mitochondria-mediated cell death pathway may be one mechanism of taurine's action against brain ischemia.
牛磺酸是神经系统中丰富的氨基酸，据报道可呈剂量依赖性减轻缺血性脑损伤。本研究旨在探讨牛磺酸是否通过影响线粒体介导的细胞死亡途径来保护大脑免受实验性中风的影响。通过管腔内细丝使大鼠经历 2 小时的缺血，然后再灌注 22 小时。再次证实，缺血后 1 小时静脉内给予牛磺酸（50mg/kg）可明显改善神经功能，并在再灌注后 22 小时减少梗死体积。在载体处理的大鼠中，缺血半暗带和核心区的细胞内 ATP 水平以及胞质和线粒体 Bcl-xL 水平明显降低，而核心区的胞质 Bax 水平和缺血半暗带和核心区的线粒体 Bax 水平显著升高。线粒体中的细胞色素 C 减少，缺血半暗带和核心区的胞质中的细胞色素 C 增加。这些变化被牛磺酸逆转。此外，牛磺酸抑制钙蛋白酶和半胱天冬酶-3 的激活，减少 αII- spectrin 的降解，并减轻缺血半暗带和核心区的坏死和凋亡性细胞死亡。这些数据表明，维持线粒体功能和阻断线粒体介导的细胞死亡途径可能是牛磺酸对抗脑缺血作用的机制之一。
