Anti-oxidative stress mechanism of velvet antler polypeptide in Alzheimer's disease model mice
10.16098/j.issn.0529-1356.2022.04.005
- Author:
Wei-Ya LANG
1
;
Tong-Hui YI
1
;
Ke-Shuang ZHANG
1
;
Hai-Yan ZHANG
1
;
Chun-Mei ZHANG
2
;
Yu-Di ZHANG
2
;
Zhong-Jin LIU
2
Author Information
1. Department of Histology and Embryology, Basic Medical College of Qiqihar Medical University
2. Department of Neurology, The First Hospital Affiliated to Qiqihar Medical College
- Publication Type:Journal Article
- Keywords:
(3-amyloid;
Alzheimer' s disease;
Antioxidant;
Mitochondria;
Mouse;
Velvet antler polypeptide;
Western blotting
- From:
Acta Anatomica Sinica
2022;53(4):432-439
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the effect of velvet antler polypeptides (VAP) on antioxidant in Alzheimer' s disease model mice. Methods Eight months old male amyloid precursor protein (APP)/presenilin-l (PS1) double transgenic mice were selected as Alzheimer' s disease (AD) model and divided into the model group and the VAP intervention group, 12 in each group. Besides, normal mice of the same brood (with no transgene) were recruited as a control group (n= 12).After 6 months of intragastric administration, behavior, morphology and oxidative stress related indicators were detected.SH-SY5 cells were used to establish AD model of damaged by Ap2535. The expression levels of APP and p-secreatase-l(BACE1) protein in mouse hippocampus were detected by Western blotting. VAP intervention group SH-SY5Y cells was cultured with VAP (500 g/L) and amyloid P(Ap) 2535(25 ixmol/L) for 24 hours. Control group cells were normally cultured by DMEM medium. Cell apoptosis, membrane potential, reactive oxygen species (ROS) levels and oxidative stress related indexes were detected. Results In animal models, compared with the model group, the escape latency of mice in the VAP intervention group was shortened (P<0. 05). The neuronal cells in the CA1 region of the hippocampus of the model group were reduced and arranged disorderly. The arrangement of the VAP intervention group was relatively regular, and the morphology was significantly improved. Compared with the model group, senile plaques were decreased in the VAP intervention group. Compared with the model group, the malondialdehyde (MDA) content ol the VAP intervention group increased, and the superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) content increased, the difference was statistically significant. Compared with the control group, the APP and BACE1 content in the model group increased. Compared with the model group, the contents of APP and BACE1 in the VAP intervention group decreased, and the difference was statistically significant (P<0. 05). In the cell model, the apoptosis rates of the VAP intervention group decreased. Compared with the model group, the mitochondrial membrane potential of the VAP intervention group increased, the content ol ROS decreased, the content of MDA decreased, and the content of SOD and GSH-Px increased. The difference were statistically significant (P<0. 05). Conclusion VAP has a protective effect on oxidative stress damage caused by Alzheimer' s disease model animals and cells, which may be achieved by reducing ROS production and increasing the activity of antioxidant enzymes to reduce Ap deposition.
