天津医药
天津醫藥
천진의약
TIANJIN MEDICAL JOURNAL
2013年
7期
686-688
,共3页
再灌注损伤%G(M1)神经节苷脂%海马%Fas配体蛋白质%大鼠, Sprague-Dawley
再灌註損傷%G(M1)神經節苷脂%海馬%Fas配體蛋白質%大鼠, Sprague-Dawley
재관주손상%G(M1)신경절감지%해마%Fas배체단백질%대서, Sprague-Dawley
reperfusion injury%G(M1) ganglioside%hippocampus%Fas ligand protein%rats,Sprague-Dawley
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Fas表达的影响。方法72只SD大鼠随机分为假手术组（8只）、GM1治疗组（32只）、缺血再灌注组（32只）。GM1治疗组和缺血再灌注组依据缺血后再灌注的不同时间点再分为6 h、12 h、24 h、3 d共4个小组。应用免疫组织化学方法和Western blot方法检测各组大鼠海马Fas蛋白的表达。结果免疫组织化学方法结果显示假手术组大鼠海马有一定量的Fas蛋白表达（0.17±0.02），而缺血再灌注组大鼠海马的Fas蛋白阳性表达显著升高，各时点分别为0.42±0.11、0.51±0.13、0.55±0.13及0.62±0.15，3 d时表达最高；与相同时间点的缺血再灌注组比较，GM1治疗组的Fas蛋白阳性表达则明显降低，各时点分别为0.29±0.09、0.34±0.11、0.37±0.12、0.43±0.12（均P<0.05）。Western blot结果与此结果类似。结论 GM1很可能通过减少Fas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Fas錶達的影響。方法72隻SD大鼠隨機分為假手術組（8隻）、GM1治療組（32隻）、缺血再灌註組（32隻）。GM1治療組和缺血再灌註組依據缺血後再灌註的不同時間點再分為6 h、12 h、24 h、3 d共4箇小組。應用免疫組織化學方法和Western blot方法檢測各組大鼠海馬Fas蛋白的錶達。結果免疫組織化學方法結果顯示假手術組大鼠海馬有一定量的Fas蛋白錶達（0.17±0.02），而缺血再灌註組大鼠海馬的Fas蛋白暘性錶達顯著升高，各時點分彆為0.42±0.11、0.51±0.13、0.55±0.13及0.62±0.15，3 d時錶達最高；與相同時間點的缺血再灌註組比較，GM1治療組的Fas蛋白暘性錶達則明顯降低，各時點分彆為0.29±0.09、0.34±0.11、0.37±0.12、0.43±0.12（均P<0.05）。Western blot結果與此結果類似。結論 GM1很可能通過減少Fas蛋白的錶達參與腦缺血再灌註損傷的神經保護作用。
목적탐토단타액산신경절감지(GM)1대뇌결혈재관주대서해마Fas표체적영향。방법72지SD대서수궤분위가수술조（8지）、GM1치료조（32지）、결혈재관주조（32지）。GM1치료조화결혈재관주조의거결혈후재관주적불동시간점재분위6 h、12 h、24 h、3 d공4개소조。응용면역조직화학방법화Western blot방법검측각조대서해마Fas단백적표체。결과면역조직화학방법결과현시가수술조대서해마유일정량적Fas단백표체（0.17±0.02），이결혈재관주조대서해마적Fas단백양성표체현저승고，각시점분별위0.42±0.11、0.51±0.13、0.55±0.13급0.62±0.15，3 d시표체최고；여상동시간점적결혈재관주조비교，GM1치료조적Fas단백양성표체칙명현강저，각시점분별위0.29±0.09、0.34±0.11、0.37±0.12、0.43±0.12（균P<0.05）。Western blot결과여차결과유사。결론 GM1흔가능통과감소Fas단백적표체삼여뇌결혈재관주손상적신경보호작용。
0bjective To study the expression of Fas in hippocampus of cerebral ischemia-reperfusion rats after treatment with monosialoganglioside (GM1). Methods Seventy-two SD rats were randomly divided into sham group (n=8), GM1 treatment group (n=32) and ischemia-reperfusion (I/R) group (n=32). According to the different time points (6 h, 12 h, 24 h and 3 d) of I/R, there were four subgroups in GM1 and I/R groups respectively. The expression of Fas in hippocampus was examined by immunochemistry and Western blot methods in all groups. Results Results of immunochemistry method showed that there was a little expression of Fas (the mean optical density was 0.17±0.02) in hippocampus of sham group, and the positive expression of Fas at different time points were increased significantly after reperfusion. The mean values of opti-cal density at different time points were 0.42±0.11, 0.51±0.13, 0.55±0.13 and 0.62±0.15 in I/R group, which reached to the peak at 3 d . The positive expression of Fas at different time points were significantly decreased in GM1 group (0.29 ± 0.09, 0.34±0.11, 0.37±0.12 and 0.43±0.12) than that of I/R group (P<0.05). Conclusion Monosialoganglioside participated in the pathogenesis of cerebral ischemia-reperfusion injury by down-regulating the expression of Fas.
