The relationship of MEOX2 and neurovascular dysfunction in Alzheimer's disease model
10.16438/j.0513-4870.2018-0633
- VernacularTitle:MEOX2基因与阿尔兹海默病神经血管功能失调的相关性研究
- Author:
Qian HE
1
;
Yi-ran CHANG
1
;
Xi KUANG
1
Author Information
1. West China School of Pharmacy, Sichuan University, Chengdu 610041, China
- Publication Type:ORIGINAL ARTICLES
- Keywords:
mesenchyme homeobox 2;
neurovascular dysfunction;
Alzheimer's disease;
low density lipoprotein receptor-related protein 1;
receptor for advanced glycation end products
- From:
Acta Pharmaceutica Sinica
2018;53(12):2057-2063
- CountryChina
- Language:Chinese
-
Abstract:
Present study investigated the role of mesenchyme homeobox 2 (MEOX2) gene in neurovascular dysfunction in Alzheimer's disease (AD) model rats by bilateral intracerebroventricular injection of Aβ1-42. One week after surgery, Morris water maze, immunohistochemistry, biochemical detection, Western blot and real-time PCR were used to detect the indexes. The animal studies were conducted in accordance with the Regulations of Experimental Animal Administration issued by the State Committee of Science and Technology of the People's Republic of China. Compared to the Sham-operated rats, Aβ1-42-operated rats showed obviously cognitive dysfunction, accompanied by increased Aβ, glial fibrillary acidic protein (GFAP), allograft inflammatory factor 1 (AIF1), endothelial nitric oxide synthase (eNOS) and decreased neuron specific enolase (NSE), synaptophysin (SYN), CD34, vascular endothelial growth factor (VEGF) expressions of brain. Aβ1-42-operated rats also increased the endothelin (ET) level and decreased nitric oxide (NO) level in brain tissue. Moreover, MEOX2 expression was decreased correlated with low density lipoprotein receptor-related protein 1 (LRP-1) decreasing and receptor for advanced glycation end products (RAGE) increasing in brain tissues of AD model rats. We found the correlation between MEOX2 gene expression and neurovascular dysfunction, in addition, the decreased MEOX2 may involve in increasing the accumulation of Aβ in brain by relating to the decreased LRP-1 and increased RAGE which is located in blood-brain barrier (BBB) in senescence-accelerated mice.
