CAJ | 학술논문

目的探讨促红细胞生成素(EPO)在脑缺血再灌注损伤中对线粒体功能的保护作用. 方法 30只SD大鼠按随机数字表法分为正常对照组、缺血再灌注组和EPO治疗组3组,每组各10只.EPO治疗组和缺血再灌注组用线栓法复制脑缺血再灌注模型.EPO治疗组在缺血再灌注后1、24、48、60 h腹腔注射EPO,剂量为3000 U/kg(用生理盐水以1:1比例稀释),缺血再灌注组腹腔注射同等剂量的生理盐水.正常对照组仅分离颈部动脉,动脉不做栓塞处理.缺血后72h观察各组大鼠脑组织神经细胞线粒体跨膜电位、线粒体丙二醛、超氧化物歧化酶、Na十_K+.ATP酶活性、一氧化氮含量和免疫组化检测海马区Caspase-3阳性细胞数的变化. 结果 EPO治疗组的神经细胞线粒体跨膜电位(77.48±5.93)、超氧化物歧化酶[(96.91±8.66)p,kat/g]、Na+_K+-ATP酶活性[(10.48±2.77)μkat/g]明显高于缺血再灌注组[44.47±17.35、(84.46±8.54)μkat/g、(7.37±2.87)μkat/g],线粒体丙二醛[(37.99±5.38)μmol/g]、一氧化氮含量[(10.18±2.02)μmol/g]、Caspase-3阳性细胞数(66.31±8.09)明显低于缺血再灌注组[(44.83±6.48)μmol/g、(12.12±2.14)μmol/g、74.90±7.42]. 结论 EPO对缺血再灌注损伤脑组织产生保护作用的重要机制之一是保护神经细胞线粒体的功能,其核心是抑制线粒体跨膜电位的下降.
목적 탐토촉홍세포생성소(EPO)재뇌결혈재관주손상중대선립체공능적보호작용. 방법 30지SD대서안수궤수자표법분위정상대조조、결혈재관주조화EPO치료조3조,매조각10지.EPO치료조화결혈재관주조용선전법복제뇌결혈재관주모형.EPO치료조재결혈재관주후1、24、48、60 h복강주사EPO,제량위3000 U/kg(용생리염수이1:1비례희석),결혈재관주조복강주사동등제량적생리염수.정상대조조부분리경부동맥,동맥불주전새처리.결혈후72h관찰각조대서뇌조직신경세포선립체과막전위、선립체병이철、초양화물기화매、Na십_K+.ATP매활성、일양화담함량화면역조화검측해마구Caspase-3양성세포수적변화. 결과 EPO치료조적신경세포선립체과막전위(77.48±5.93)、초양화물기화매[(96.91±8.66)p,kat/g]、Na+_K+-ATP매활성[(10.48±2.77)μkat/g]명현고우결혈재관주조[44.47±17.35、(84.46±8.54)μkat/g、(7.37±2.87)μkat/g],선립체병이철[(37.99±5.38)μmol/g]、일양화담함량[(10.18±2.02)μmol/g]、Caspase-3양성세포수(66.31±8.09)명현저우결혈재관주조[(44.83±6.48)μmol/g、(12.12±2.14)μmol/g、74.90±7.42]. 결론 EPO대결혈재관주손상뇌조직산생보호작용적중요궤제지일시보호신경세포선립체적공능,기핵심시억제선립체과막전위적하강.
Objective To investigate the protective effect of erythropoietin(EPO)on the mitochondria in the brain neurons against cerebral ischemia/reperfusion(IR)injury in rats.Methods Thirty SD rats are randomly allocated into 3 groups,namely the EPO group(n=10),IR group(n=10),and shamoperation group(n=10).In EPO group and IR group,the rats were subjected to middle cerebral artery occlusion(MCAO)to induce cerebral IR injury,followed by treatment with intraperitonal EPO injection at 3000 U/kg and the same volume of saline,respectively.In the sham operation group,the carofid artery was only isolated without MCAO or subsequent treatment.Seventy-two hours after the IR injury,the mitochondrial membrane potential in the neurons was detected,and the changes in superoxide kismutase(SOD)activity,malondialdehyde(MDA)and nitric oxide(NO)concentrations,and Na+-K+-ATPase activity in the neuronal mitochondria were determined.The number of caspase-3-positive neurons in the hippocampus Was observed immunohistochemically. Results The mitochondrial membrane potential and activities of SOD and Na+-K+-ATPase Were significantly higher.whereas the MDA and NO concentrations and the number of caspase-3-postive neurons significantly lower in EPO group than in IR group after the treatment.Conclusion Protecting the neuronal mitochondrial function is one of the important mechanisms of EPO for brain protection against IR injury,and this mitochondrial protection effect is mediated essentially by stabilizing the mitochondrial membrane potential.