Effects of polygonatum polysaccharide on p38 MAPK/N-cadherin in zebrafish with Alzheimer disease
10.3867/j.issn.1000-3002.2021.10.075
- Author:
Yi-Fei CHEN
1
;
Kai-Fei LIU
;
Shi-Min WU
;
Xun-Yi LI
;
Yao HUANG
;
Dian-Feng HUANG
;
Cai-Wu JIANG
Author Information
1. Guilin Medical University,Guilin 541199,China
- Keywords:
Alzheimer disease;
zebrafish;
polygonatum polysaccharide;
N-cadherin;
p38 MAPK
- From:
Chinese Journal of Pharmacology and Toxicology
2021;35(10):760-760
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To study the effect of polygonatum polysaccharide on zebrafish with Alzheimer disease. METHODS Zebrafish were trained in T maze for 7 d. The 40 zebrafish successfully trained were divided into 4 groups:blank group, model group, positive group and polygonatum polysaccharide group. Model group, positive group and polygonatum polysaccharide group were put in AlCl3100μg·L-1 for 6 d. The positive group was exposed to Huperzine A solution 4μg·L-1, and the polygonatum polysaccharide group was exposed to polygonatum polysaccharide solution 6 g·L-1 for 6 d. The model group was not treated, and the blank group was not treated. Each stage of zebrafish was recorded by video, and the time of each group in the EC region was analyzed. After administration, the brain tissue was taken out and the expression of N-cadherin, P38 and p-P38 protein factors was determined by Western blotting. RESULTS In behavior, the analysis of the time spent in the EC area, the blank group, the positive group and the polygonatum polysac?charide group were compared with the model group, respectively, there were statistically significant differences (P<0.05). At the protein level, compared with the model group, the P38 and p-P38 proteins in the positive group and the polygonatum polysaccharide group were down-regulated, while the N-cadherin protein was up-regulated, with statistical difference (P<0.05). CONCLUSION Polygonatum polysaccharide can improve the learning and memory ability of zebrafish with Alzheimer disease by up regulating the protein level of N-cadherin and hindering P38 phosphorylation.
