临床神经病学杂志
臨床神經病學雜誌
림상신경병학잡지
JOURNAL OF CLINICAL NEUROLOGY
2015年
2期
121-124
,共4页
王红霞%李世英%李峥%张晋霞%贺永贵%余红%孙妍%刘斌
王紅霞%李世英%李崢%張晉霞%賀永貴%餘紅%孫妍%劉斌
왕홍하%리세영%리쟁%장진하%하영귀%여홍%손연%류빈
缺血预处理%脑缺血再灌注%低氧诱导因子-1α%存活素%脑缺血耐受
缺血預處理%腦缺血再灌註%低氧誘導因子-1α%存活素%腦缺血耐受
결혈예처리%뇌결혈재관주%저양유도인자-1α%존활소%뇌결혈내수
ischemic preconditioning%cerebral ischemia reperfusion%hypoxia-inducible factor-1α%survi-vin%cerebral ischemia tolerance
目的:探讨缺血预处理对局灶性脑缺血再灌注大鼠缺血侧海马CA1区低氧诱导因子-1α( HIF-1α)及存活素表达的影响。方法健康雄性SD大鼠130只随机分为假手术组( SO组,n=10)、局灶性脑缺血再灌注组( MCAO组,n=60)、缺血预处理组( BIP组,n=60),MCAO组和BIP组又分别分为再灌注2 h、6 h、12 h、24 h、48 h、72 h 6个亚组,每亚组10只大鼠。采用线栓法制备大鼠脑缺血再灌注模型。 BIP组在缺血前24 h给予10 min的预缺血。采用免疫组化染色法检测HIF-1α、存活素的阳性细胞数。采用Western blot法检测HIF-1α、存活素的蛋白相对含量。结果与SO组比较,MCAO组和BIP组各时间点亚组大鼠缺血侧海马CA1区HIF-1α及存活素的阳性细胞数及蛋白相对含量均明显升高(均P<0.05)。与MCAO组比较,BIP组各时间点亚组大鼠缺血侧海马CA1区HIF-1α及存活素的阳性细胞数及蛋白相对含量均明显升高(均P<0.05)。在MCAO组和BIP组中,大鼠缺血侧海马CA1区HIF-1α及存活素的阳性细胞数及蛋白相对含量均在再灌注24 h时达到最高峰(均P<0.05)。结论缺血预处理能够诱导局灶性脑缺血再灌注大鼠缺血侧海马CA1区HIF-1α、存活素表达上调,这或许与脑缺血耐受的产生机制有关。
目的:探討缺血預處理對跼竈性腦缺血再灌註大鼠缺血側海馬CA1區低氧誘導因子-1α( HIF-1α)及存活素錶達的影響。方法健康雄性SD大鼠130隻隨機分為假手術組( SO組,n=10)、跼竈性腦缺血再灌註組( MCAO組,n=60)、缺血預處理組( BIP組,n=60),MCAO組和BIP組又分彆分為再灌註2 h、6 h、12 h、24 h、48 h、72 h 6箇亞組,每亞組10隻大鼠。採用線栓法製備大鼠腦缺血再灌註模型。 BIP組在缺血前24 h給予10 min的預缺血。採用免疫組化染色法檢測HIF-1α、存活素的暘性細胞數。採用Western blot法檢測HIF-1α、存活素的蛋白相對含量。結果與SO組比較,MCAO組和BIP組各時間點亞組大鼠缺血側海馬CA1區HIF-1α及存活素的暘性細胞數及蛋白相對含量均明顯升高(均P<0.05)。與MCAO組比較,BIP組各時間點亞組大鼠缺血側海馬CA1區HIF-1α及存活素的暘性細胞數及蛋白相對含量均明顯升高(均P<0.05)。在MCAO組和BIP組中,大鼠缺血側海馬CA1區HIF-1α及存活素的暘性細胞數及蛋白相對含量均在再灌註24 h時達到最高峰(均P<0.05)。結論缺血預處理能夠誘導跼竈性腦缺血再灌註大鼠缺血側海馬CA1區HIF-1α、存活素錶達上調,這或許與腦缺血耐受的產生機製有關。
목적:탐토결혈예처리대국조성뇌결혈재관주대서결혈측해마CA1구저양유도인자-1α( HIF-1α)급존활소표체적영향。방법건강웅성SD대서130지수궤분위가수술조( SO조,n=10)、국조성뇌결혈재관주조( MCAO조,n=60)、결혈예처리조( BIP조,n=60),MCAO조화BIP조우분별분위재관주2 h、6 h、12 h、24 h、48 h、72 h 6개아조,매아조10지대서。채용선전법제비대서뇌결혈재관주모형。 BIP조재결혈전24 h급여10 min적예결혈。채용면역조화염색법검측HIF-1α、존활소적양성세포수。채용Western blot법검측HIF-1α、존활소적단백상대함량。결과여SO조비교,MCAO조화BIP조각시간점아조대서결혈측해마CA1구HIF-1α급존활소적양성세포수급단백상대함량균명현승고(균P<0.05)。여MCAO조비교,BIP조각시간점아조대서결혈측해마CA1구HIF-1α급존활소적양성세포수급단백상대함량균명현승고(균P<0.05)。재MCAO조화BIP조중,대서결혈측해마CA1구HIF-1α급존활소적양성세포수급단백상대함량균재재관주24 h시체도최고봉(균P<0.05)。결론결혈예처리능구유도국조성뇌결혈재관주대서결혈측해마CA1구HIF-1α、존활소표체상조,저혹허여뇌결혈내수적산생궤제유관。
Objective To observe the effects of ischemic preconditioning on the expression of hypoxia-inducible factor-1α( HIF-1α) and survivin at ischemia bilateral hippocampal CA1 area in rats with focal cerebral ischemia reperfusion.Methods One hundred and thirty healthy male SD rats were randomly divided into sham operation group ( SO group, n =10 ) , focal cerebral ischemia reperfusion group ( MCAO group, n =60 ) and ischemia preconditioning group ( BIP group, n=60) .The MCAO group and BIP group were further divided into reperfusion 2 h, 6 h, 12 h, 24 h, 48 h and 72 h 6 subgroups, respectively, with 10 rats in each subgroup.Sutured method was used to made focal cerebral ischemia reperfusion model rats.The BIP group received ischemic preconditioning with 10 min at 24 h before cerebral ischemia.The numbers of positive cells of HIF-1αand survivin were detected by immunohistochemistry.The relative contents of protein of HIF-1αand survivin were detected by Western blot method.Results Compared with the SO group, the numbers of positive cells and the relative contents of protein of HIF-1α, survivin at ischemia bilateral hippocampal CA1 area in subgroups at each time point of MCAO group and BIP group were significantly increased ( all P<0.05 ) .Compared with the MCAO group, the numbers of positive cells and the relative contents of protein of HIF-1α, survivin at ischemia bilateral hippocampal CA1 area in subgroups at each time point of BIP group were significantly increased ( all P<0.05) .In the MCAO group and BIP group, the numbers of positive cells and the relative contents of protein of HIF-1α, survivin at ischemia bilateral hippocampal CA1 area were all arrived the peak at reperfusion 24 h moment ( all P<0.05 ) .Conclusions Ischemic preconditioning can increase the expression of HIF-1α, survivin at ischemia bilateral hippocampal CA1 area in rats with focal cerebral ischemia reperfusion.It may be related to the mechanism of cerebral ischemia tolerance.