Amyloid P oligomer promotes microglial galectin-3 and astrocytic lipocalin-2 levels in the hippocampus of mice fed a high-fat diet

被引:2
作者
Shin, Hyun Joo [1 ]
Kim, Kyung Eun [1 ]
Jeong, Eun Ae [1 ]
An, Hyeong Seok [1 ]
Lee, So Jeong [1 ]
Lee, Jaewoong [1 ]
Roh, Gu Seob [1 ,2 ]
机构
[1] Gyeongsang Natl Univ, Inst Hlth Sci, Coll Med, Dept Anat & Convergence Med Sci, Jinju 52727, South Korea
[2] Gyeongsang Natl Univ, Coll Med, Dept Anat, 15 Jinju Daero 816 Beon Gil, Jinju Si 52727, Gyeongnam, South Korea
基金
新加坡国家研究基金会;
关键词
Galectin-3; Lipocalin-2; Astrocyte; Microglia; Hippocampus; Diabetes; Alzheimer's disease; OXIDATIVE STRESS; NEUROINFLAMMATION;
D O I
10.1016/j.bbrc.2023.05.026
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Type 2 diabetes is associated with a risk factor for Alzheimer's disease (AD). Activation of glial cells, such as microglia and astrocytes, is crucial for the development of neuroinflammation in both diabetes and AD. The role of amyloid-beta oligomer (APO) in the hippocampus of diabetic mice has been investigated; however, the effect of galectin-3 and lipocalin-2 (LCN2) on amyloid toxicity-related glial activation in diabetic mice is not known. To fill this knowledge gap, we fed mice a high-fat diet (HFD) for 20 weeks to induce a diabetic state and then injected the hippocampus with APO. Sholl analysis of iba-1-positive microglia showed retraction of microglial ramifications in the hippocampus of HFD-fed diabetic mice. APO treatment caused more retraction of microglial process in HFD-fed mice. In particular, microglial galectin-3 levels and astrocytic LCN2 levels were increased in the hippocampus of HFD-fed mice with APO treatment. These findings suggest that galectin-3 and LCN2 are involved in amyloid toxicity mechanisms, especially glial activation under diabetic conditions. (c) 2023 Elsevier Inc. All rights reserved.
引用
收藏
页码:10 / 17
页数:8
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