中华神经医学杂志
中華神經醫學雜誌
중화신경의학잡지
CHINESE JOURNAL OF NEUROMEDICINE
2008年
5期
449-452
,共4页
马德选%王晓强%卞留贯%沈建康
馬德選%王曉彊%卞留貫%瀋建康
마덕선%왕효강%변류관%침건강
GPR40%脑缺血%猴%多元不饱和脂肪酸%海马
GPR40%腦缺血%猴%多元不飽和脂肪痠%海馬
GPR40%뇌결혈%후%다원불포화지방산%해마
GPR40%Ischemia%Monkey%Polyunsaturated fatty acid%Hippocampus
目的 利用猴短暂性全脑缺血模型,研究蛋白偶联受体40(GPR40)在海马的表达,从而探讨GPR40受体在缺血性卒中的作用.方法 参照Yamashima建立成年猴短暂性全脑缺血模型,24只猴随机数字表法分成4组,即对照组、缺血后4 d组(d4)、缺血后9 d组(d9)和缺血后15 d(d15),采用Western印迹和免疫荧光在蛋白质水平观察GPR40的表达.结果 Western blotting结果显示CA1区域GPR40在短暂性全脑缺血后表达逐渐下降(15 d内);而在DG区域表达升高,与对照组比较有统计学意义(P<0.05).免疫荧光分析显示CA1区域与GPR40共表达的神经元细胞数逐渐下降.到d15约下降50%;而DG区域则无明显变化,邻近SGZ区域与GPR40共表达的星形细胞数量迅速升高,d4升高约2.5倍.结论 脑缺血后海马CA1和DG两区域GPR40表达差异.特别SGZ星形细胞GPR40表达升高,提示可通过增加GPR40配体中长链不饱和脂肪酸如DHA来改善脑缺血后海马神经元的损伤.
目的 利用猴短暫性全腦缺血模型,研究蛋白偶聯受體40(GPR40)在海馬的錶達,從而探討GPR40受體在缺血性卒中的作用.方法 參照Yamashima建立成年猴短暫性全腦缺血模型,24隻猴隨機數字錶法分成4組,即對照組、缺血後4 d組(d4)、缺血後9 d組(d9)和缺血後15 d(d15),採用Western印跡和免疫熒光在蛋白質水平觀察GPR40的錶達.結果 Western blotting結果顯示CA1區域GPR40在短暫性全腦缺血後錶達逐漸下降(15 d內);而在DG區域錶達升高,與對照組比較有統計學意義(P<0.05).免疫熒光分析顯示CA1區域與GPR40共錶達的神經元細胞數逐漸下降.到d15約下降50%;而DG區域則無明顯變化,鄰近SGZ區域與GPR40共錶達的星形細胞數量迅速升高,d4升高約2.5倍.結論 腦缺血後海馬CA1和DG兩區域GPR40錶達差異.特彆SGZ星形細胞GPR40錶達升高,提示可通過增加GPR40配體中長鏈不飽和脂肪痠如DHA來改善腦缺血後海馬神經元的損傷.
목적 이용후단잠성전뇌결혈모형,연구단백우련수체40(GPR40)재해마적표체,종이탐토GPR40수체재결혈성졸중적작용.방법 삼조Yamashima건립성년후단잠성전뇌결혈모형,24지후수궤수자표법분성4조,즉대조조、결혈후4 d조(d4)、결혈후9 d조(d9)화결혈후15 d(d15),채용Western인적화면역형광재단백질수평관찰GPR40적표체.결과 Western blotting결과현시CA1구역GPR40재단잠성전뇌결혈후표체축점하강(15 d내);이재DG구역표체승고,여대조조비교유통계학의의(P<0.05).면역형광분석현시CA1구역여GPR40공표체적신경원세포수축점하강.도d15약하강50%;이DG구역칙무명현변화,린근SGZ구역여GPR40공표체적성형세포수량신속승고,d4승고약2.5배.결론 뇌결혈후해마CA1화DG량구역GPR40표체차이.특별SGZ성형세포GPR40표체승고,제시가통과증가GPR40배체중장련불포화지방산여DHA래개선뇌결혈후해마신경원적손상.
Objective To investigate the expression of free fatty acid receptor GPR40 and evaluate the possible function of GPR40 in the adult monkey hippocampus after ischemia. Methods According to the post-ischemic adult monkey model of Yamashima, a total of 24 adult monkeys were randomly divided into 4 groups: sham-operated group (control) and post-ischemic day 4, 9, 15 (d4, d9,d15). The expression of free fatty acid receptor GPR40 was detected at the protein level by immunoblotting and immunohistochemistry in the adult monkey hippocampus. Results Immunoblotting analysis showed the expression of GPR40 was decreased in CA1 and increased in DG after ischemia (posfischemic group vs control, P＞0.05). Immunohistochemistry data revealed that the double stained cells of GPR40 and NeuN were also decreased by 50% (d15) in CA1 and had no significant changes in DG after ischemia. Interestingly, the co-labeled cells of GPR40 and GFAP were increased 2.5 folds (d4) in post-ischemic SGZ. Conclusions There is the different expression of GPR40 in adult monkey hippocampal CA1 and DG regions after ischemia. Co-labeled cells of GPR40 and GFAP are increased in post-ischemic SGZ, which indicates that polyunsaturated free fatty acid such as DHA, a ligand of GPR40, may alleviate neuronal injury in post-ischemic hippocampus.
