Effect of rehabilitation training on insulin-resistance and hippocampus amyloid-beta peptide in rats with vascular dementia.
10.3969/j.issn.1672-7347.2013.11.014
- Author:
Hongwei WANG
1
;
Qing YE
;
Yan HUANG
;
Huiying LIAO
;
Haifen HUANG
;
Yong YOU
Author Information
1. Department of Neurology, First Affiliated Hospital of Nanhua University, Hengyang Hunan 421001, China 965188402@qq.com.
- Publication Type:Journal Article
- MeSH:
Amyloid beta-Peptides;
analysis;
Animals;
Dementia, Vascular;
therapy;
Drugs, Chinese Herbal;
Female;
Hippocampus;
enzymology;
Insulin;
blood;
Insulin Resistance;
Insulysin;
analysis;
Learning;
Memory;
Rats;
Rats, Sprague-Dawley
- From:
Journal of Central South University(Medical Sciences)
2013;38(11):1167-1171
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the effect of rehabilitation training on insulin-resistance and insulin degrading enzyme (IDE) in the hippocampus in rats with vascular dementia.
METHODS:A total of 45 female Sprague-Dawley rats were randomly assigned into a rehabilitation group (n=15), an immobilization group (n=15), and a sham-operation group (n=15). The rats in the former 2 groups were operated on to establish the experimental vascular dementia model by bilateral common carotid artery permanent ligation. The rats' learning and memory were assessed 4 weeks after the operation. The plasma level of insulin was determined by ELISA at different time points after the operation. Immunohistochemical staining was used to detect the IDE expression in the hippocampus area.
RESULTS:The rats in the rehabilitation group showed significantly better learning ability than that in the immobilization group (P<0.05). The plasma level of insulin in the rehabilitation group was lower than that in the immobilization group (P<0.05), IDE expression in the rehabilitation group was higher than that in the immobilization group (P<0.05) at 7 d and 28 d after the operation.
CONCLUSION:Rehabilitation can accelerate the recovery of learning and memory in rats with vascular dementia, and the mechanism is possibly related to the amelioration of insulin resistance and increase of IDE expression in the hippocampus.
