口服PTD-SOD对大鼠局灶性脑缺血再灌注损伤的保护作用

目的探讨口服灌胃PTD．SOD对大鼠局灶性脑缺血再灌注（cerebral ischemia-reperfusion，CIR）引起的脑损伤的保护作用及机制。方法采用线栓法制作大鼠大脑中动脉闭塞再灌注模型（middl ecerebral artery occlusion，MCAO），缺血2h，再灌注24h。于缺血前一周开始灌胃给予PTD-SOD10，20，40mg·kg-1，2次d-1。对术后MCAO大鼠进行神经行为学特性观察并评分；TTC染色法测量大鼠脑梗死面积；生化法检测大鼠脑组织匀浆中s0D、GSH-Px、CAT的活力和MDA、NO的含量。HE染色观察大鼠脑组织病理改变。结果PTD．SOD可明显改善大鼠神经行为，减少脑梗死面积，提高脑内SOD、GSH-Px、CAT的活性，降低脑组织中MDA及N0含量，减轻脑组织病理改变（P〈0．05或P〈O．01）。结论PTD．SOD可减轻CIR神经细胞损伤，其机制可能与其能抗自由基损伤，减轻NO神经毒性有关。

Protection of Fusion Protein PTD-SOD by Oral on Rats of Focal Cerebral Ischemia/Reperfusion Injury

OBJECTIVE To investigate the protection mechanism of fusion protein PTD-SOD on damaged cerebral tissues by studying the effect of PTD-SOD on cerebral ischemia-reperfusion(CIR) of rats. METHODS To establish middle cerebral artery occlusion models with middle cerebral artery thread embolism method for two-hour ischemia and twenty-four-hour reperfusion, to observe variations of areas of cerebral infarction by TTC staining method, to measure changes/variations of indices of anti-oxidative system and oxidative levels of cerebral homogenate of rats, and the damage situation of cerebral cells were tested by paraffin sections and HE staining. RESULTS Compared with model groups, the areas of cerebral infarction of administration groups were much smaller, the levels of antioxidative indices of cerebral tissuse, such as SOD, GSH-PX and CAT, were significantly increased, while the level of MDA was significantly decreased. At the same time, HE staining showed the damage situation of cerebral cells of administrtion groups were less than cerebral cells of model groups. CONCLUSION Oral administration of PTD-SOD is able to improve levels of anti free radical effect on cerebral tissuse, as well as lessen cerebral infarction and decrease the damage situation of cerebral cells of ischemia reperfusion rats.