茶氨酸对脑缺血损伤大鼠自由基代谢的影响

目的:从对自由基代谢影响方面探讨茶氨酸对脑缺血损伤的保护作用机制。方法:选用30只SD雄性大鼠,线栓阻塞大鼠大脑中动脉制备局灶性脑缺血模型,观察脑缺血损伤大鼠神经症状改变,测定脑组织含水量、脑组织病理及钙离子含量;观察其血清和脑组织超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量变化以及茶氨酸对上述变化的影响。结果:脑缺血组大鼠的神经症状评分、脑组织含水量及钙离子含量均显著增高,病理损伤明显,正常神经元细胞数目减少;茶氨酸可显著降低神经症状评分、脑组织含水量及钙离子含量,增加正常神经元细胞数目。脑缺血组大鼠的血清、脑组织SOD活性显著降低,茶氨酸组大鼠血清、脑组织SOD活性较脑缺血组显著增高;脑缺血组大鼠的血清、脑组织MDA含量显著增高,茶氨酸组脑组织MDA含量较脑缺血组下降明显。结论:茶氨酸对大鼠脑缺血损伤具有显著的保护作用,可能与调节脑缺血损伤引起的自由基代谢失调有关。

Effects of theanine on free radical metabolism in rats with ischemic brain injury

Objective To explore the mechanism of protective action of theanine in cerebral ischemic injury via detecting changes in free radical metabolism. Methods 30 male SD rats were randomized to sham-operated group, ischemia-reperfusion group, or theanine group. The rat model of focal cerebral ischemia was constructed by nylon thread occlusion of the middle cerebral artery. The changes of neural symptoms in the rats were observed; the contents of water and Ca2 and the pathological alterations in the brain tissues were determined; the changes of serum superoxide dismutase (SOD)activity and malondialdehyde (MDA) content and the effects of theanine were observed. Results In the ischemia-reperfusion group, neurological deficit scores and the contents of water and Ca2 were significantly increased,pathologic injury was obvious, and the number of normal neurons was reduced. However, theanine significantly decreased the scores and the contents of water and Ca2 and increased the number of normal neurons. The SOD activities in both serum and brain tissues were markedly declined in the ischemia-reperfusion group but significantly increased in the theanine group as compared to the ischemia-reperfusion group. The MDA contents in both serum and brain tissues were notably elevated in the ischemia-reperfusion group while significantly decreased in the theanine group as compared to the ischemia-reperfusion group. Conclusions Theanine has a significant protective effect on cerebral ischemic injury in rats, which may be associated with its regulatory effect on the imbalance of free radical metabolism due to ischemic injury.