重庆医学
重慶醫學
중경의학
CHONGQING MEDICAL JOURNAL
2014年
17期
2113-2115
,共3页
邹磊%刘丹彦%殷薇%宋云
鄒磊%劉丹彥%慇薇%宋雲
추뢰%류단언%은미%송운
高压氧%缺血预处理%老龄%轴突生长抑制因子%轴突生长抑制因子受体A
高壓氧%缺血預處理%老齡%軸突生長抑製因子%軸突生長抑製因子受體A
고압양%결혈예처리%노령%축돌생장억제인자%축돌생장억제인자수체A
hyperbaric-oxygenation%ischemic-preconditioning%aged%Nogo%Nogo-A
目的:研究高压氧预处理对老龄大鼠全脑缺血再灌注损伤时轴突生长抑制因子(Nogo)mRNA、Nogo-A蛋白表达的影响,探讨其影响神经可塑性的机制。方法将42只雄性 SD大鼠分为4组:对照组(C组,n=6)、高压氧组(H 组,n=12)、脑缺血再灌注损伤组(I/R组,n=12)、高压氧预处理+脑缺血再灌注损伤组(HOP组,n=12)。H 组和 HOP组每天置于高压氧舱内1 h,氧压为0.2 MPa,连续5 d,最后1次高压氧处理后24 h时 I/R组和 HOP组采用改良Pulsinelli四血管闭塞法制备大鼠全脑缺血再灌注损伤模型,全脑缺血10 min,再灌注24 h时 H组、I/R组和 HOP组随机取6只大鼠断头取脑,分离大脑皮质,采用实时荧光定量PCR法检测 Nogo mRNA的表达水平,免疫印迹法检测 Nogo-A蛋白的表达水平。各组大鼠分别行横断位及冠状位T1WI、T2WI扫描。结果 C组、H组大脑未见明显缺血梗死灶,缺血组双侧皮质区可见明显弧形缺血梗死区,HOP组双侧皮质区也可见弧形缺血梗死区,面积较 I/R组小。与C组比较,Nogo mRNA及 Nogo-A蛋白表达上调(P<0.05);与 I/R组比较, Nogo mRNA及 Nogo-A蛋白表达下调(P<0.05)。结论高压氧预处理通过抑制大脑皮质Nogo mRNA及Nogo-A蛋白表达上调,提高神经可塑性,能减少老龄大鼠急性全脑缺血后超急性期大脑皮质缺血梗死面积。
目的:研究高壓氧預處理對老齡大鼠全腦缺血再灌註損傷時軸突生長抑製因子(Nogo)mRNA、Nogo-A蛋白錶達的影響,探討其影響神經可塑性的機製。方法將42隻雄性 SD大鼠分為4組:對照組(C組,n=6)、高壓氧組(H 組,n=12)、腦缺血再灌註損傷組(I/R組,n=12)、高壓氧預處理+腦缺血再灌註損傷組(HOP組,n=12)。H 組和 HOP組每天置于高壓氧艙內1 h,氧壓為0.2 MPa,連續5 d,最後1次高壓氧處理後24 h時 I/R組和 HOP組採用改良Pulsinelli四血管閉塞法製備大鼠全腦缺血再灌註損傷模型,全腦缺血10 min,再灌註24 h時 H組、I/R組和 HOP組隨機取6隻大鼠斷頭取腦,分離大腦皮質,採用實時熒光定量PCR法檢測 Nogo mRNA的錶達水平,免疫印跡法檢測 Nogo-A蛋白的錶達水平。各組大鼠分彆行橫斷位及冠狀位T1WI、T2WI掃描。結果 C組、H組大腦未見明顯缺血梗死竈,缺血組雙側皮質區可見明顯弧形缺血梗死區,HOP組雙側皮質區也可見弧形缺血梗死區,麵積較 I/R組小。與C組比較,Nogo mRNA及 Nogo-A蛋白錶達上調(P<0.05);與 I/R組比較, Nogo mRNA及 Nogo-A蛋白錶達下調(P<0.05)。結論高壓氧預處理通過抑製大腦皮質Nogo mRNA及Nogo-A蛋白錶達上調,提高神經可塑性,能減少老齡大鼠急性全腦缺血後超急性期大腦皮質缺血梗死麵積。
목적:연구고압양예처리대노령대서전뇌결혈재관주손상시축돌생장억제인자(Nogo)mRNA、Nogo-A단백표체적영향,탐토기영향신경가소성적궤제。방법장42지웅성 SD대서분위4조:대조조(C조,n=6)、고압양조(H 조,n=12)、뇌결혈재관주손상조(I/R조,n=12)、고압양예처리+뇌결혈재관주손상조(HOP조,n=12)。H 조화 HOP조매천치우고압양창내1 h,양압위0.2 MPa,련속5 d,최후1차고압양처리후24 h시 I/R조화 HOP조채용개량Pulsinelli사혈관폐새법제비대서전뇌결혈재관주손상모형,전뇌결혈10 min,재관주24 h시 H조、I/R조화 HOP조수궤취6지대서단두취뇌,분리대뇌피질,채용실시형광정량PCR법검측 Nogo mRNA적표체수평,면역인적법검측 Nogo-A단백적표체수평。각조대서분별행횡단위급관상위T1WI、T2WI소묘。결과 C조、H조대뇌미견명현결혈경사조,결혈조쌍측피질구가견명현호형결혈경사구,HOP조쌍측피질구야가견호형결혈경사구,면적교 I/R조소。여C조비교,Nogo mRNA급 Nogo-A단백표체상조(P<0.05);여 I/R조비교, Nogo mRNA급 Nogo-A단백표체하조(P<0.05)。결론고압양예처리통과억제대뇌피질Nogo mRNA급Nogo-A단백표체상조,제고신경가소성,능감소노령대서급성전뇌결혈후초급성기대뇌피질결혈경사면적。
Objective To investigate the effect of hyperbaric oxygen preconditioning (HOP)on expression of Nogo mRNA,No-go-A and Ng R protein in the cerebral cortex after acute global cerebral ischemia-reperfusion (I/R)in aged rats and to study its mechanism affecting neuroplasticity.Methods Forty-two aged male SD rats were randomly divided into 4 groups:control group (C group,n=6),hyperbaric oxygen group (H group,n=12),cerebral I/R injury group (I/R group,n=12)and HOP group (n=12). The H group and the HOP group were placed in the hyperbaric oxygen cabin for 1 h per day with a oxygen pressure of 0.2 Mpa for successive 5 d,at 24 h after last time of hyperbaric oxygen preconditioning the I/R group and the HOP group adopted the modified Pulsinelli vessel occlusion method for preparing the rat I/R injury model,with global cerebral ischemia for 10 min and reperfusion for 24 h,each 6 rats were randomly taken from the the H group,I/R group and HOP group and their heads were cut off for taking the brain and isolating the cerebral cortex.The real time fluorescence quantification PCR was adopted to detect the expression level of Nogo mRNA and the Nogo-A protein level was detected by Western blot.The rats in various groups were performed the T1 WI and T2WI scanning in the transection position and the coronal positions.Results There were no obvious ischemic brain infarction in the normal control group and the H group,the arc-shaped bilateral cortex ischemic infarct area was clearly seen in the ischemic group,the ischemic infarct area was also seen in the HOP ischemia group,but its area was smaller than which in the ischemic group.Compared with the C group,the expression of Nogo mRNA and the Nogo-A protein in the HOP group was up-regulated(P<0.05);compared with the I/R group,the expression of Nogo mRNA and the Nogo-A protein was down-regulated(P<0.05). Conclusion HOP increases the neuroplasticity and can reduce the cerebral ischemic infarction area in the exceed acute stage of rat acute global cerebral ischemia by inhibiting Nogo mRNA in the cerebral cortex and up-regulating the Nogo-A protein expression.