CAJ | 학술논문

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。
목적관찰문동안산갑대대서국조성뇌결혈재관주후신경세포조망적보호작용。 　　방법채용웅성SD대서우측대뇌중동맥폐새모형，결혈2 h，재관주22 h。대서수궤분위5조，매조10지，재결혈후1 h경복강주사급여생리염수（1 ml/kg）혹불동제량문동안산갑（10 mg/kg、25 mg/kg、62.5 mg/kg화125 mg/kg），관찰불동제량문동안산갑대대서뇌결혈재관주후신경공능결손화경사체적적영향。령취32지대서수궤분위용제대조조화문동안산갑조，재결혈후1 h복강주사생리염수（1 ml/kg）혹문동안산갑（62.5 mg/kg），동시설립가수술조16지，검측삼조대서뇌조직삼린산선감（adenosine triphosphate，ATP）화유산수평（매조10지），이급조망성세포정황（매조6지）。 　　결과여용제대조조비교，62.5 mg/kg제량적문동안산갑능현저개선신경공능결손（P<0.001），강저경사체적（P=0.011）；여용제대조조비교，25 mg/kg제량적문동안산갑능감소경사체적（P=0.040），단신경공능평분무차이；10 mg/kg화125 mg/kg제량적문동안산갑조신경공능평분화경사체적여용제대조조균무차이。여용제대조조비교，문동안산갑（62.5 mg/kg）능감소ATP적하강（P=0.036）화세포조망（P<0.001）。 　　결론문동안산갑대대서국조성뇌결혈재관주후적세포조망유보호작용。
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 deifcits 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.