摘要
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。
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 rain 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 ratio of rats with focal cerebral I/R injury. Compared with apocynin group , apocynin combined with PKCinhibitor 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.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2015年第8期1126-1131,共6页
Chinese Pharmacological Bulletin
基金
国家自然科学基金资助项目(No 81402930)
安徽省自然科学基金资助项目(No 1408085MH176)
