CAJ | 학술논문

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。
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.