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CJAP ›› 2016, Vol. 32 ›› Issue (3): 193-197.doi: 10.13459/j.cnki.cjap.2016.03.001

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The effects of H102 on NF-κB signal pathway in brain of transgenic AD mice

WANG Chao, YUAN Xiao-yong, SUN Feng-xian, JIANG Fang, XU Shu-mei   

  1. Department of Physiology, Tianjin Medical University, Tianjin 300070, China
  • Received:2016-01-08 Revised:2016-02-11 Online:2016-05-28 Published:2018-06-12
  • Supported by:
    国家科技重大专项基金资助(2009ZX09103-029);天津市科技支撑重点项目基金资助(09ZCKFSH00100)

Abstract: Objective:To investigate the effects of β-sheet breaker peptide H102 on NF-κB signal pathway in brain of APP/PS1 double transgenic mice. Methods:Thirty 8-week-old APP/PS1 double transgenic mice were randomly divided into model group and treatment group. A group of C57BL/6J mice with the same age and background were served as controls (n=15). H102 5 μl(5.8 mg/kg) was infused by intranasal administration to mice in H102 treatment group, and equal volume of blank solution of H102 (chitosan, BSA) was given to mice in control group and model group. After 16 weeks, the ability of spatial reference memory was tested by Morris Water Maze. Then immunohistochemistry tests and Western blot technique were used to detect the content of amyloid beta peptide 1-42(Aβ1-42), nuclear factor-kappa B (NF-κB), inhibitor of NF-κB (IκB), IκB kinase (IKK), the corresponding phosphorylated proteins (p-NF-κB、p-IκB、p-IKK), inducible nitric oxide synthase (iNOS) and cleaved Caspase 3 proteins in mice brain. Results:①The ability of learning and memory was significantly lowered in model group than that in control group. And the ability of learning and memory was significantly improved in treatment group than that in model group (P<0.05). ②The contents of Aβ1-42, p-IKK, p-NF-κB, p-IκB, intranuclear NF-κB,iNOS and cleaved Caspase 3 in mouse brain were significantly increased in model group than those of control group, and these protein expressions were significantly lowered in treatment group than those in model group (P<0.05). Conclusion:H102 can inhibit NF-κB signal pathway in brain of APP/PS1 double transgenic mice, reduce the levels of inflammation and apoptosis in nerve cells, and improve the ability of learning and memory in transgenic AD mice.

Key words: Alzheimer disease, mice, transgenic, H102, NF-κB signal pathway

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