CAJ | 학술논문

目的：研究抑制 NADPH 氧化酶对大鼠局灶性脑缺血/再灌注损伤的保护作用及可能机制。方法利用线栓法制备大鼠大脑中动脉栓塞( middle cerebral artery occlusion, MCAO)模型,于缺血前15 min尾静脉注射apocynin 2．5 mg ·kg-1,脑缺血2 h恢复血液再灌注24 h后,对大鼠进行神经行为学评分、脑梗死体积、脑组织病理形态学以及Cx36、PKC、Bax、Bcl-2蛋白表达变化的检测。结果使用NADPH氧化酶抑制剂apocynin,能明显降低局灶性脑缺血/再灌注损伤大鼠神经行为学评分和脑梗死体积百分率,减轻脑组织病理形态学损伤,增加大鼠Cx36、PKC蛋白的表达,降低Bax与Bcl-2的比值。在使用apocynin的基础上加用PKC激酶抑制剂,与单用 apocynin组相比,其上述保护作用则减弱。结论抑制NADPH氧化酶能够减轻脑缺血/再灌注损伤,并且能增高Cx36、PKC的蛋白表达,降低Bax与Bcl-2的比值。
목적：연구억제 NADPH 양화매대대서국조성뇌결혈/재관주손상적보호작용급가능궤제。방법이용선전법제비대서대뇌중동맥전새( middle cerebral artery occlusion, MCAO)모형,우결혈전15 min미정맥주사apocynin 2．5 mg ·kg-1,뇌결혈2 h회복혈액재관주24 h후,대대서진행신경행위학평분、뇌경사체적、뇌조직병리형태학이급Cx36、PKC、Bax、Bcl-2단백표체변화적검측。결과사용NADPH양화매억제제apocynin,능명현강저국조성뇌결혈/재관주손상대서신경행위학평분화뇌경사체적백분솔,감경뇌조직병리형태학손상,증가대서Cx36、PKC단백적표체,강저Bax여Bcl-2적비치。재사용apocynin적기출상가용PKC격매억제제,여단용 apocynin조상비,기상술보호작용칙감약。결론억제NADPH양화매능구감경뇌결혈/재관주손상,병차능증고Cx36、PKC적단백표체,강저Bax여Bcl-2적비치。
Aim To determine the protective effect of NADPH oxidase against focal cerebral ischemia/reper-fusion ( I/R) injury in rats. Method A thread occlu-sion method was used to make a middle cerebral artery occlusion ( MCAO ) model. Apocynin ( 2. 5 mg · kg-1 ) was injected by tail vein 15 min before ischemi-a. Then, the neurological behavior, cerebral infarction volume, pathological morphological changes and the expression of Cx36, PKC, Bax, Bcl-2 of rats were de-tected after ischemia for 2 h, followed by reperfusion for 24 h. Results Compared with cerebral I/R group, administration of apocynin significantly reduced the neurological behavior scores and the cerebral in-farction volume percentage, alleviated the pathological morphological damage, increased the protein expres-sion of Cx36 and PKC, and reduced the Bax/Bcl-2 ra-tio of rats with focal cerebral I/R injury. Compared with apocynin group , apocynin combined with PKC inhibitor significantly reduced above protective effects. Conclusion Inhibition of NADPH oxidase could alle-viate cerebral I/R injury, increase the levels of Cx36, PKC proteins and reduce the Bax/Bcl-2 ratio.