Role of TXNIP-mediated oxidative stress in delaying Alzheimer's disease by estrogen.
10.11817/j.issn.1672-7347.2019.180667
- Author:
Qiong PAN
1
;
Ke GUO
2
;
Yaqian LI
3
;
Qiuyun TU
3
Author Information
1. Department of Obstetrics and Gynecology, Third Xiangya Hospital, Central South University, Changsha 410013, China.
2. Department of Neurology, Third Xiangya Hospital, Central South University, Changsha 410013, China.
3. Department of Geriatrics, Third Xiangya Hospital, Central South University, Changsha 410013, China.
- Publication Type:Journal Article
- MeSH:
Alzheimer Disease;
Animals;
Carrier Proteins;
Cell Cycle Proteins;
Estrogens;
Hippocampus;
Oxidative Stress;
Rats;
Reactive Oxygen Species
- From:
Journal of Central South University(Medical Sciences)
2019;44(12):1360-1366
- CountryChina
- Language:Chinese
-
Abstract:
To study the functional mechanism of thioredoxin-interacting protein (TXNIP) in delaying Alzheimer's disease (AD) by estrogen.
Methods: After estradiol (E2) treatment in Aβ-induced AD cell model, reactive oxygen species (ROS), TXNIP, and apoptosis levels were detected. After lentiviral infection with TXNIP overexpression, the effect of E2 on ROS and apoptosis were observed. In the AD rat model, the learning and memory ability and the expression of TXNIP in the hippocampus were observed in the presence of E2. After overexpressing TXNIP, the effect of E2 on the learning and memory ability of AD rat model was observed.
Results: ROS, TXNIP and apoptosis levels were enhanced in AD cell model, while E2 treatment reduced ROS, TXNIP and apoptosis levels in AD cell model. After enhancing TXNIP, E2 treatment reduced ROS and apoptosis levels in AD cell model. Similar to the cell experiment, E2 enhanced the learning and memory ability in the AD rat model and inhibited the expression of TXNIP in brain, while TXNIP overexpression attenuated the effect of E2 on learning and memory ability in the AD rats.
Conclusion: Estrogen can inhibit the expression of TXNIP in nerve tissue, reduce nerve damage, and delay the development of AD.
