山西医药杂志
山西醫藥雜誌
산서의약잡지
SHANXI MEDICAL JOURNAL
2014年
22期
2625-2627
,共3页
关仲阳%刘婷%刘宇兵%郑家涛%杜江
關仲暘%劉婷%劉宇兵%鄭傢濤%杜江
관중양%류정%류우병%정가도%두강
脑缺血%再灌注损伤%神经节苷脂%P38丝裂原活化蛋白激酶%大鼠
腦缺血%再灌註損傷%神經節苷脂%P38絲裂原活化蛋白激酶%大鼠
뇌결혈%재관주손상%신경절감지%P38사렬원활화단백격매%대서
Brain ischemia injury%Reperfusion injury%G (M1) Ganglioside%P38 mitogen-activated protein kinase%Rats
目的:探讨单唾液酸神经节苷脂(GM 1)对脑缺血再灌注大鼠海马丝裂原活化蛋白激酶(MAPK)表达的影响。方法72只SD大鼠按随机数字表法分为:假手术组(Sham组,8只)、GM1治疗组(GM1组,32只)、缺血再灌注组(I/R组,32只)。G M 1治疗组和I/R组依据缺血后再灌注的不同时间点再细分为6 h ,12h,24h,3d4个小组。应用免疫组织化学方法和蛋白印迹法检测各组大鼠海马MAPK蛋白的表达。结果免疫组织化学方法检测时发现,MAPK在Sham组大鼠海马即有表达,缺血处理后,MAPK表达迅速增高,在6 h时表达已经接近峰值,之后持续激活,至12 h时最高,24 h表达降低,3 d时表达较Sham组仍显著升高;与相同时间点的缺血组比较,GM1治疗组的MAPK蛋白阳性表达则明显降低( P <0.05);蛋白印迹法也得到了相同的结论。结论 GM1很可能通过减少MAPK蛋白的表达参与脑缺血再灌注损伤的神经保护作用。
目的:探討單唾液痠神經節苷脂(GM 1)對腦缺血再灌註大鼠海馬絲裂原活化蛋白激酶(MAPK)錶達的影響。方法72隻SD大鼠按隨機數字錶法分為:假手術組(Sham組,8隻)、GM1治療組(GM1組,32隻)、缺血再灌註組(I/R組,32隻)。G M 1治療組和I/R組依據缺血後再灌註的不同時間點再細分為6 h ,12h,24h,3d4箇小組。應用免疫組織化學方法和蛋白印跡法檢測各組大鼠海馬MAPK蛋白的錶達。結果免疫組織化學方法檢測時髮現,MAPK在Sham組大鼠海馬即有錶達,缺血處理後,MAPK錶達迅速增高,在6 h時錶達已經接近峰值,之後持續激活,至12 h時最高,24 h錶達降低,3 d時錶達較Sham組仍顯著升高;與相同時間點的缺血組比較,GM1治療組的MAPK蛋白暘性錶達則明顯降低( P <0.05);蛋白印跡法也得到瞭相同的結論。結論 GM1很可能通過減少MAPK蛋白的錶達參與腦缺血再灌註損傷的神經保護作用。
목적:탐토단타액산신경절감지(GM 1)대뇌결혈재관주대서해마사렬원활화단백격매(MAPK)표체적영향。방법72지SD대서안수궤수자표법분위:가수술조(Sham조,8지)、GM1치료조(GM1조,32지)、결혈재관주조(I/R조,32지)。G M 1치료조화I/R조의거결혈후재관주적불동시간점재세분위6 h ,12h,24h,3d4개소조。응용면역조직화학방법화단백인적법검측각조대서해마MAPK단백적표체。결과면역조직화학방법검측시발현,MAPK재Sham조대서해마즉유표체,결혈처리후,MAPK표체신속증고,재6 h시표체이경접근봉치,지후지속격활,지12 h시최고,24 h표체강저,3 d시표체교Sham조잉현저승고;여상동시간점적결혈조비교,GM1치료조적MAPK단백양성표체칙명현강저( P <0.05);단백인적법야득도료상동적결론。결론 GM1흔가능통과감소MAPK단백적표체삼여뇌결혈재관주손상적신경보호작용。
Objective To study the expression of mitogen‐activated protein kinase(MAPK) in hippocampus of cerebral ischemia‐reperfusion rats after monosialoganglioside was injected .Methods Seventy‐two SD rats were randomly divided into the sham group ,ischemia‐reperfusion group(I/R) ,monosialoganglioside group(GM1) at different time points (6 h ,12 h ,24 h ,3 d) after reperfusion on average .The expression of MAPK in hippocampus of all groups was examined by immunochemistry and Western blotting methods .Results We found the positive ex‐pression of MAPK in hippocampus of the rats in sham group by immunochemistry method ,and the positive ex‐pression of MAPK was increased significantly as soon as monosialoganglioside was injected ( P<0 .05) ,then the expression of MAPK sustained a high level ,to the peak at 12 h ,decreased at 24 h ,and higher significantly com‐pared with the sham group at 3 d;compared with the rats of the I/R group at the same time point ,the positive ex‐pression of MAPK decreased significantly in GM 1 group ( P<0 .05);and the same result was obtained by West‐ern blotting method .Conclusion One of the mechanisms for monosialoganglioside participating the pathogenesis of cerebral ischemia‐reperfusion injury might be downregulating the expression of MAPK.