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《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:

22卷

期数:

2016年05期

页码:

396-400

栏目:

基础医学

出版日期:

2016-09-20

文章信息/Info

Title:

Effects of β-sheet breaker peptide H102 on LPL and PPAR-γ protein in double transgenic AD mice

文章编号:

1006-8147（2016）05-0396-05

作者:

?李 靖; 付雪斐; 孙凤仙; 袁小涌; 王 超; 徐淑梅

（天津医科大学生理学教研室，天津 300070）

Author(s):

?LI Jing;  FU Xue-fei;  SUN Feng-xian;  YUAN Xiao-yong;  WANG Chao;  XU Shu-mei

?（Department of Physiology, Tianjin Medical University, Tianjin 30070, China）

关键词:

β片层阻断肽; 阿尔茨海默症; LPL; PPAR-γ;  PS1/ APP 双转基因小鼠

Keywords:

β-Sheet breaker peptide-H102; Alzheimer’s disease; LPL; PPAR-γ;  PS1/ APP transgene mice

分类号:

R338

DOI:

-

文献标志码:

A

摘要:

目的：通过观察β片层阻断肽H102对PS1/APP双转基因AD模型小鼠学习记忆能力以及脑中LPL及PPAR表达的影响，探究H102对阿尔茨海默病(AD)治疗作用的可能机制。 方法：将AD模型小鼠随机分为模型组和H102治疗组，并将同月龄同背景C57BL/6J小鼠设为正常对照组，H102治疗组小鼠鼻腔给予H102药液，5 μL/d；模型组及正常组小鼠鼻腔给予辅料溶液，5 μL/d。连续给药4周后进行Morris水迷宫测试，检测小鼠学习记忆能力，并应用实时定量荧光PCR（Real-Time PCR）技术、Western Blot技术以及免疫组化法，观察小鼠脑内LPL 和PPAR-γ表达的改变。 结果： Real-Time PCR技术、Western Blot技术以及免疫组化法均显示，与模型组小鼠相比，H102治疗组小鼠脑内LPL和PPAR-γ的表达显著增加(P＜0.05)。 结论：β片层阻断肽H102能够增加AD小鼠脑内LPL的表达，从而进一步促进Aβ的细胞内吞与降解，而在这个过程中，PPAR-γ可能参与其中。

Abstract:

Objective ：To observe the effects of H102 on the learning ability and memory of PS1/APP transgenic AD mice and the expression of LPL and PPAR-γ. Methods： PS1/APP transgenic AD mice were randomly divided into two groups：model group and control group，while C57BL/6J mice were normal group. The treatment group received 33 mg/mL liquid for 5 μL/d，while the normal group and model group were given with an equal volume of materials solution for 4 weeks. After that，the Spatial learning ability and memory was tested by Morris Water Maze. Immunohistochemical test，Western blotting and quantitative real-time PCR were used to test the expression of LPL. The quantitative real-time PCR and immunohistochemical test were also used to examine the expression of PPAR-γ. Results： Immunohistochemical test，Western blotting and quantitative real-time PCR indicated the expression of LPL and PPAR-γ in the model group were decreased significantly than the H102 group (P<0.05). Conclusion：It’s found that H102 can improve the ability of learning and memory in PS1/APP transgenic AD mice. It’s also indicated that β-sheet breaker peptide-H102 may work via regulating the expression of LPL so as to promote the degradation of Aβ， and PPAR-γ may be involved in the procedure. Those findings also prove that LPL in the brain may be highly correlated with the pathogenesis of AD.

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相似文献/References:

[1]付雪斐,李 靖,孙凤仙,等.β片层阻断肽对AD模型小鼠学习记忆及PI3K/AKT信号通路的影响[J].天津医科大学学报,2016,22(05):391.
　FU Xue-fei,LI Jing,SUN Feng-xian,et al. Effect of β-sheet breaker peptide on learning and memory and PI3K /AKT? signaling pathway in AD model mice ? [J].Journal of Tianjin Medical University,2016,22(05):391.

备注/Memo

备注/Memo:

作者简介 李靖（1990-），女，硕士在读，研究方向：生理学；

通信作者：徐淑梅：E-mail: xushm@tijmu.edu.cn。