中华神经医学杂志
中華神經醫學雜誌
중화신경의학잡지
CHINESE JOURNAL OF NEUROMEDICINE
2012年
4期
337-341
,共5页
葛宇松%尹琳%滕伟禹%张朝东
葛宇鬆%尹琳%滕偉禹%張朝東
갈우송%윤림%등위우%장조동
阿尔茨海默病%β-淀粉样蛋白%亲环素A%细胞凋亡
阿爾茨海默病%β-澱粉樣蛋白%親環素A%細胞凋亡
아이자해묵병%β-정분양단백%친배소A%세포조망
AD%Amyloid beta-protein%Cyclophilin A%Apoptosis
目的 探讨Aβ25-35对大鼠海马神经元的损伤及对亲环素A(CyPA)表达的影响. 方法 健康Wister大鼠60只按照随机数字表法分为实验组(n=30)和对照组(n-30),实验组大鼠采用Aβ25-35注射入双侧海马制造阿尔茨海默病的动物模型,对照组大鼠同样位置注射入等量生理盐水.HE染色观察2组大鼠海马CA1区神经元形态,TUNEL染色检测细胞凋亡,RT-PCR检测CyPAmRNA的表达,Western blotting检测CyPA蛋白的表达. 结果 实验组大鼠海马CA1区神经元遭到破坏,细胞凋亡增加,数量减少,且随时间延长细胞凋亡情况进一步加重,造模后1d、7d、14d较对照组比较差异均有统计学意义(P＜0.05).实验组大鼠海马组织CyPA mRNA和CyPA蛋白表达量随时间呈现出先增长后降低的趋势,1d、7d时明显高于对照组,差异均有统计学意义(P＜0.05).14d时明显低于对照组大鼠,其中CyPA蛋白的差异具有统计学意义(P＜0.05). 结论 Aβ25-35通过加重大鼠海马神经元凋亡诱发神经毒性作用,CyPA表达的增加可能是一种内源性保护因素.
目的 探討Aβ25-35對大鼠海馬神經元的損傷及對親環素A(CyPA)錶達的影響. 方法 健康Wister大鼠60隻按照隨機數字錶法分為實驗組(n=30)和對照組(n-30),實驗組大鼠採用Aβ25-35註射入雙側海馬製造阿爾茨海默病的動物模型,對照組大鼠同樣位置註射入等量生理鹽水.HE染色觀察2組大鼠海馬CA1區神經元形態,TUNEL染色檢測細胞凋亡,RT-PCR檢測CyPAmRNA的錶達,Western blotting檢測CyPA蛋白的錶達. 結果 實驗組大鼠海馬CA1區神經元遭到破壞,細胞凋亡增加,數量減少,且隨時間延長細胞凋亡情況進一步加重,造模後1d、7d、14d較對照組比較差異均有統計學意義(P＜0.05).實驗組大鼠海馬組織CyPA mRNA和CyPA蛋白錶達量隨時間呈現齣先增長後降低的趨勢,1d、7d時明顯高于對照組,差異均有統計學意義(P＜0.05).14d時明顯低于對照組大鼠,其中CyPA蛋白的差異具有統計學意義(P＜0.05). 結論 Aβ25-35通過加重大鼠海馬神經元凋亡誘髮神經毒性作用,CyPA錶達的增加可能是一種內源性保護因素.
목적 탐토Aβ25-35대대서해마신경원적손상급대친배소A(CyPA)표체적영향. 방법 건강Wister대서60지안조수궤수자표법분위실험조(n=30)화대조조(n-30),실험조대서채용Aβ25-35주사입쌍측해마제조아이자해묵병적동물모형,대조조대서동양위치주사입등량생리염수.HE염색관찰2조대서해마CA1구신경원형태,TUNEL염색검측세포조망,RT-PCR검측CyPAmRNA적표체,Western blotting검측CyPA단백적표체. 결과 실험조대서해마CA1구신경원조도파배,세포조망증가,수량감소,차수시간연장세포조망정황진일보가중,조모후1d、7d、14d교대조조비교차이균유통계학의의(P＜0.05).실험조대서해마조직CyPA mRNA화CyPA단백표체량수시간정현출선증장후강저적추세,1d、7d시명현고우대조조,차이균유통계학의의(P＜0.05).14d시명현저우대조조대서,기중CyPA단백적차이구유통계학의의(P＜0.05). 결론 Aβ25-35통과가중대서해마신경원조망유발신경독성작용,CyPA표체적증가가능시일충내원성보호인소.
Objective To explore the neuron injury in rat hippocampus induced by Aβ25-35 and the cyclophilin A (CyPA) expression changes in these neurons. Methods Sixty healthy Wister rats were equally randomized into experimental group and control group (n=30); AD rat models in the experimental group were established by injection of Aβ25-35 into the bilateral hippocampus of rats,and rats of the control group were received NS injection. The morphological features of neurons in the CA1 area of hippocampus were observed by HE staining; the neuron apoptosis was determined with TUNEL staining; the mRNA and protein expressions of CyPA were detected by PT-PCR and Western blotting,respectively. Results Aβ25-35 caused damage and apoptosis of neurons in the CA1 area of hippocampus; with time being prolonged,the cell injury aggravated and apoptosis increased in the CA1 area ofhippocampus; significant differences were noted as compared with those in control group 1,7 and 14 d after the inducement (P＜0.05).After injection of Aβ25-35 into the hippocampus of rat,the mRNA and protein expressions of CyPA were obviously changed:in early stage,the expressions increased,and then,the expressions decreased gradually; significant differences were noted as compared with those in control group 1 and 7 d after the inducement (P＜0.05); the protein expression of CyPA in the experimental group 14 d after the inducement was significantly decreased as compared with that in the control group (P＜0.05). Conclusion Aβ25-35 plays a neurotoxicity role through aggravating the apoptosis of neurons; and the increment of CyPA expressions maybe play an endogenously protective role in these damage.
