RETRACTED: Protective Effects of Colivelin Against Alzheimer's Disease in a PDAPP Mouse Model (Retracted article. See vol. 56, pg. 315, 2022)

被引:10
|
作者
Yin, Rong [1 ]
Yin, Kai [2 ]
Guo, ZhiQiang [3 ]
Zhang, ZhiQiang [1 ]
Chen, LiPin [1 ]
Cao, Li [1 ]
Li, YuanMin [1 ]
Wei, YaXuan [1 ]
Fu, XueFeng [4 ]
Shi, XiangQu [1 ]
机构
[1] Lanzhou Gen Hosp Lanzhou Mil Command, Dept Neurol, Lanzhou, Peoples R China
[2] 281 Hosp Peoples Liberat Army, Dept Dept Clin Lab, Qinhuangdao, Peoples R China
[3] Lanzhou Gen Hosp Lanzhou Mil Command, Phys Examinat Ctr, Lanzhou, Peoples R China
[4] Lanzhou Gen Hosp Lanzhou Mil Command, Dept Carder Ward, Lanzhou, Peoples R China
基金
中国国家自然科学基金;
关键词
Alzheimers's disease; Colivelin; Memory dysfunction; p38 signaling pathway; AMYLOID-BETA; TAU-PROTEIN; HUMANIN; PEPTIDE; IMPAIRMENT; DEPOSITION; MECHANISM; CYTOKINES; CASPASE-3; MEMORY;
D O I
10.1159/000443064
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Background: Alzheimer's disease (AD) is characterized with progressive memory loss and severe cognitive impairments, which affect everyday life and human health in the elderly. It is required that an effective and safe protective reagent against AD should be developed. It has been reported that humanin (HN) exerts neuroprotective effects against AD. In this study, we investigated the effect of a novel and more effective HN derivative, Colivelin (CLN) on AD. Methods: PDAPPV717I transgenic AD model mice (derived from parental C57/ BL6 mice) were used in our study as AD model. Morris water maze test was used to test the memory impairment of AD mice and the levels of A beta 40 and A beta 42 were determined by an Elisa assay. We used an Immunohistochemistry and Immunofluorescence staining method to check the GFAP and MAP2 positive cells, and TUNEL to assess the apoptotic cells. Western blot assay was used to check the expression and phosphorylation level of p38. Results: We found that CLN improved the memory impairment induced by AD and reduced the deposit of A beta 40 and A beta 42. CLN also inhibited cell apoptosis and activation of caspase 3 in brain tissues of AD mice. Inflammation in AD mice was alleviated by CLN treatment, including the accumulation of GFAP positive cells and the inflammatory cytokines. With both structure of AGA-HNG and ANDF, CLN exhibited significantly stronger effects than synchronously administration of AGA-HNG and ADNF, suggesting CLN as a novel potential effective therapeutic reagent for AD patients. Finally, we found that CLN inhibited phosphorylation of p38 in AD mice and p38 inhibitor, SB203580 weakened the therapeutic effect of CLN. Conclusion: CLN effectively improved the memory dysfunction in PDAPP mice, and our data suggests CLN as a novel and effective reagent which may have great potentials in AD therapy. (C) 2016 The Author(s) Published by S. Karger AG, Basel
引用
收藏
页码:1138 / 1146
页数:9
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