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目的本文应用依达拉奉与脑蛋白水解物治疗慢性脑缺血实验研究,通过观测丙二醛(MDA)和超氧化物歧化酶(SOD)的含量探讨慢性脑缺血治疗的有效性。方法线结扎离断法制作大鼠颈动脉的局灶性慢性脑缺血模型,造模3 w后给予依达拉奉3 mg/kg腹腔注射,于不同时间点用卒中指数评分标准和神经病学症状标准评估大鼠神经功能损伤程度,用各实验组大鼠脑组织匀浆测定MDA和SOD的含量。结果脑缺血模型鼠卒中指数1～3 d死亡率为35%～38.9%,显著高于正常对照组;脑缺血4 w MDA含量升高明显,12 w恢复正常,依达拉奉和脑蛋白水解物组与正常对照组、脑缺血模型组比差异有显著性(P<0.01),且脑蛋白水解物MDA含量增加不如依达拉奉组显著(P<0.01);脑缺血模型组和给药组在4 w时SOD含量明显减少,依达拉奉组和脑蛋白水解物组在8 w、12 w额叶皮层与海马区SOD的表达均显著高于脑缺血模型组(P<0.01),且依达拉奉组各时点SOD的含量均高于脑蛋白水解物组(P<0.01),但16 w后SOD含量恢复正常,脑缺血模型组在12 w时额叶皮质及海马区SOD含量明显低于正常对照组(P<0.01)。结论慢性脑缺血是痴呆的病理基础,梗死灶多发生在缺血的2～4 w,以分水岭区较多见;依达拉奉具有抑制缺血后血管内皮细胞损害,清除自由基、抑制脑水肿,影响单胺类神经递质的代谢,而发挥神经保护作用,其有效性优于脑蛋白水解物。
Objective To study the therapeutic effect of edaravone and brain protein hydrolyzate on chronic cerebral ischemia in rats. The therapeutic effect of chronic cerebral ischemia was investigated by observing the content of malondialdehyde (MDA) and superoxide dismutase (SOD). Methods The model of focal chronic cerebral ischemia in rat carotid artery was made by the method of line ligation and disconnection. After 3 weeks, edaravone 3 mg / kg was injected intraperitoneally, and at different time points, the stroke index score and neurology Symptom criteria were evaluated for the extent of neurological impairment in rats, and the content of MDA and SOD in the brain tissue of each experimental group was measured. Results The mortality of cerebral infarction index in 1 ~ 3 days was 35% ~ 38.9% in cerebral ischemia model rats, which was significantly higher than that in normal control group. The MDA content in cerebral ischemia rats increased significantly at 4 w and returned to normal after 12 weeks. Compared with normal control group and cerebral ischemia model group, the protein hydrolyzate group had significant difference (P <0.01), and the increase of MDA content of brain protein hydrolyzate was not as significant as that of edaravone group (P <0.01) SOD and SOD in hippocampus of 8 w and 12 w frontal cortex and hippocampus were significantly higher in group Edaravone and brain protein hydrolyzate than that in group of cerebral ischemia (P <0.01). The content of SOD in edaravone group was higher than that in brain protein hydrolyzate group at each time point (P <0.01), but SOD level returned to normal after 16 w, SOD in the cortex and hippocampus was significantly lower than that in the normal control group (P <0.01). Conclusion Chronic cerebral ischemia is the pathological basis of dementia. Infarct mostly occurs in 2 ~ 4 w of ischemia, which is more common in the watershed. Edaravone can inhibit the damage of vascular endothelial cells after ischemia, scavenge free radicals and inhibit Brain edema, affecting the metabolism of monoamine neurotransmitters, and play a neuroprotective effect, its effectiveness is superior to brain protein hydrolysates.