门冬氨酸钾对局灶性脑缺血再灌注大鼠的保护作用研究

目的 观察门冬氨酸钾对大鼠局灶性脑缺血再灌注后神经细胞凋亡的保护作用。 方法 采用雄性SD大鼠右侧大脑中动脉闭塞模型，缺血2 h，再灌注22 h。大鼠随机分为5组，每组10 只，在缺血后1 h经腹腔注射给予生理盐水（1 ml/kg）或不同剂量门冬氨酸钾（10 mg/kg、25 mg/kg、 62.5 mg/kg和125 mg/kg），观察不同剂量门冬氨酸钾对大鼠脑缺血再灌注后神经功能缺损和梗死 体积的影响。另取32只大鼠随机分为溶剂对照组和门冬氨酸钾组，在缺血后1 h腹腔注射生理盐水 （1 ml/kg）或门冬氨酸钾（62.5 mg/kg），同时设立假手术组16只，检测三组大鼠脑组织三磷酸腺苷 （adenosine triphosphate，ATP）和乳酸水平（每组10只），以及凋亡性细胞情况（每组6只）。 结果 与溶剂对照组比较，62.5 mg/kg剂量的门冬氨酸钾能显著改善神经功能缺损（P <0.001）， 降低梗死体积（P =0.011）；与溶剂对照组比较，25 mg/kg剂量的门冬氨酸钾能减少梗死体积 （P =0.040），但神经功能评分无差异；10 mg/kg和125 mg/kg剂量的门冬氨酸钾组神经功能评分和 梗死体积与溶剂对照组均无差异。与溶剂对照组比较，门冬氨酸钾（62.5 mg/kg）能减少ATP的下降 （P =0.036）和细胞凋亡（P <0.001）。 结论 门冬氨酸钾对大鼠局灶性脑缺血再灌注后的细胞凋亡有保护作用。

Protective Effects of Potassium Aspartate on Focal Cerebral Ischemia/Reperfusion in Rats

Objective To investigate the protection of potassium aspartate (PA) against focal cerebral ischemia/
reperfusion in rats.
Methods Male Sprague-Dawley rats were subjected to 2 h of right middle cerebral artery occlusion
(MCAO) and 22 h of reperfusion. Rats were randomly divided into 5 groups, 10 rats in each group.
Saline (1 ml/kg) or different doses of PA (10 mg/kg, 25 mg/kg, 62.5 mg/kg and 125 mg/kg) was
administrated intraperitoneally after 1 h MCAo, to observe the effects of PA at different dosage
on neurological deficits and infarct volume after cerebral ischemia/reperfusion in rats. Another 32
rats were assigned to vehicle group and PA group randomly, at 1 h after ischemia by intraperitoneal
injection of saline (1 ml/kg) or PA (62.5 mg/kg). Sixteen rats were used as the sham operation group.
Brain adenosine triphosphate (ATP) and lactic acid levels (n =10), and the apoptotic cell death (n =6)
were evaluated.
Results PA treatment at the dose of 62.5 mg/kg significantly improved neurological deficits
(P <0.001) and decreased the infarct volume compared with vehicle treatment (P =0.011); compared
with vehicle treatment, PA treatment at the dose of 25 mg/kg dose can reduce the infarct volume
markedly (P =0.040), but no differences in neurological deficits; both neurological deficits and
infarct volume were improved following 10 mg/kg and 125 mg/kg PA in comparison to vehicle,
although it was not significant. PA treatment (62.5 mg/kg) significantly reduced the loss of ATP
(P =0.036), and the apoptotic cell death (P <0.001) compared with vehicle treatment.
Conclusion PA has neuroprotective effects against apoptosis after cerebral ischemia/reperfusion in rats.