南方医科大学学报
南方醫科大學學報
남방의과대학학보
JOURNAL OF SOUTHERN MEDICAL UNIVERSITY
2014年
3期
323-328
,共6页
邓炎尧%侯德仁%田密%李维%奉夏露
鄧炎堯%侯德仁%田密%李維%奉夏露
산염요%후덕인%전밀%리유%봉하로
阿尔茨海默病%淀粉样蛋白%microRNA%小脑
阿爾茨海默病%澱粉樣蛋白%microRNA%小腦
아이자해묵병%정분양단백%microRNA%소뇌
Alzheimer disease%amyloid%microRNA%cerebellum
目的:通过对比观察AD模型小鼠海马与小脑Aβ沉积和相关miRNAs表达的变化,探讨AD模型小鼠小脑是否存在Aβ沉积和相关miRNAs的差异表达。方法选择12月龄大小的APPswe/PS△E9双转基因AD小鼠作为实验组(EG),同月龄的同种系的野生型小鼠C57为对照组(CG),每组各12只。将小鼠脑组织分为左右两部分,右侧脑组织行刚果红染色检测淀粉样物质在海马及小脑的沉积;左侧脑组织分别用于提取海马及小脑的miRNA,应用实时荧光定量PCR方法分别检测两组小鼠海马及小脑组织的miRNA-135a-5p、miRNA-298-5p、miRNA-466b-3p和miR-669f-3p的表达情况。结果刚果红染色:实验组小鼠海马及小脑均可见橘红色的Aβ沉积,对照组小鼠海马及小脑均未见橘红色的Aβ沉积。实时荧光定量PCR:四种miRNAs在实验组海马的表达均低于对照组(P<0.05);miRNA-135a-5p、miRNA-298-5p和miR-669f-3p在实验组小脑的表达低于对照组(P<0.05);miRNA-298-5p和miR-669f-3p在实验组海马的表达低于小脑(P<0.05)。结论APPswe/PS△E9双转基因AD小鼠小脑中也存在Aβ沉积,其形成可能与miRNA-135a-5p、miRNA-298-5p和miR-669f-3p的表达下调有关。
目的:通過對比觀察AD模型小鼠海馬與小腦Aβ沉積和相關miRNAs錶達的變化,探討AD模型小鼠小腦是否存在Aβ沉積和相關miRNAs的差異錶達。方法選擇12月齡大小的APPswe/PS△E9雙轉基因AD小鼠作為實驗組(EG),同月齡的同種繫的野生型小鼠C57為對照組(CG),每組各12隻。將小鼠腦組織分為左右兩部分,右側腦組織行剛果紅染色檢測澱粉樣物質在海馬及小腦的沉積;左側腦組織分彆用于提取海馬及小腦的miRNA,應用實時熒光定量PCR方法分彆檢測兩組小鼠海馬及小腦組織的miRNA-135a-5p、miRNA-298-5p、miRNA-466b-3p和miR-669f-3p的錶達情況。結果剛果紅染色:實驗組小鼠海馬及小腦均可見橘紅色的Aβ沉積,對照組小鼠海馬及小腦均未見橘紅色的Aβ沉積。實時熒光定量PCR:四種miRNAs在實驗組海馬的錶達均低于對照組(P<0.05);miRNA-135a-5p、miRNA-298-5p和miR-669f-3p在實驗組小腦的錶達低于對照組(P<0.05);miRNA-298-5p和miR-669f-3p在實驗組海馬的錶達低于小腦(P<0.05)。結論APPswe/PS△E9雙轉基因AD小鼠小腦中也存在Aβ沉積,其形成可能與miRNA-135a-5p、miRNA-298-5p和miR-669f-3p的錶達下調有關。
목적:통과대비관찰AD모형소서해마여소뇌Aβ침적화상관miRNAs표체적변화,탐토AD모형소서소뇌시부존재Aβ침적화상관miRNAs적차이표체。방법선택12월령대소적APPswe/PS△E9쌍전기인AD소서작위실험조(EG),동월령적동충계적야생형소서C57위대조조(CG),매조각12지。장소서뇌조직분위좌우량부분,우측뇌조직행강과홍염색검측정분양물질재해마급소뇌적침적;좌측뇌조직분별용우제취해마급소뇌적miRNA,응용실시형광정량PCR방법분별검측량조소서해마급소뇌조직적miRNA-135a-5p、miRNA-298-5p、miRNA-466b-3p화miR-669f-3p적표체정황。결과강과홍염색:실험조소서해마급소뇌균가견귤홍색적Aβ침적,대조조소서해마급소뇌균미견귤홍색적Aβ침적。실시형광정량PCR:사충miRNAs재실험조해마적표체균저우대조조(P<0.05);miRNA-135a-5p、miRNA-298-5p화miR-669f-3p재실험조소뇌적표체저우대조조(P<0.05);miRNA-298-5p화miR-669f-3p재실험조해마적표체저우소뇌(P<0.05)。결론APPswe/PS△E9쌍전기인AD소서소뇌중야존재Aβ침적,기형성가능여miRNA-135a-5p、miRNA-298-5p화miR-669f-3p적표체하조유관。
Objective To investigate the presence of β-amyloid peptide (Aβ) deposition in the cerebellum and the expression of related miRNAs in the cerebellum of a mouse model of Alzheimer disease. Methods Twelve 12-month-old APPswe/PS△E9 double transgenic mice and 12 wild-type C57 mice were sacrificed and the brain tissues were taken for examination. The right hemisphere was stained with Congo red to observe the deposition of amyloid substances, and from the left hemisphere, the hippocampus and the cerebellum were dissected for detecting the expression of miRNA-135a-5p, miRNA-298-5p, miRNA-466b-3p and miR-669f-3p using real-time PCR. Results Congo red staining revealed the presence of Aβdeposition in both the hippocampus and the cerebellum of the transgenic mice but not in the control mice. Real-time PCR showed a significantly lower expression of the 4 miRNAs in the hippocampus in the transgenic mice than in the control mice (P<0.05). The expression of miRNA-135a-5p, miRNA-298-5p, and miR-669f-3p in the cerebellum was significantly lower in the transgenic mice than in the control mice (P<0.05). The expression of miRNA-298-5p and miR-669f-3p in the hippocampus was significantly lower than that in the cerebellum of the transgenic mice (P<0.05). Conclusion Aβdeposition also occurs in the cerebellum of APPswe/PS△E9 double transgenic mice, and its formation might be related to the down-regulation of miRNA-135a-5p, miRNA-298-5p, and miR-669f-3p.