Dihydromyricetin improves Parkinson's disease-like lesions in T2DM rats by activating AMPK/ULK1 pathway.
- Author:
Qi LI
1
;
Nian CHEN
2
;
Jin-Ding LUO
1
;
Hui-Lin WU
3
;
Zi-Han WANG
1
;
Meng-Wei LI
1
;
Shui-Dong FENG
4
;
Hong-Yan LING
5
Author Information
1. Department of Physiology, Hengyang Medical College, University of South China, Hengyang 421001, China.
2. Department of Medical Cosmetology, the First Affiliated Hospital, University of South China, Hengyang 421001, China.
3. Clinical Medicine Class 10, Grade 2018, Hengyang Medical College, University of South China, Hengyang 421001, China.
4. Department of Social Medicine and Health Management, School of Public Health, University of South China, Hengyang 421001, China. shuidong-f@hotmail.com.
5. Department of Physiology, Hengyang Medical College, University of South China, Hengyang 421001, China. linghongyan0203@126.com.
- Publication Type:Journal Article
- MeSH:
Rats;
Animals;
Parkinson Disease;
Rats, Sprague-Dawley;
AMP-Activated Protein Kinases;
Diabetes Mellitus, Type 2;
Autophagy-Related Protein-1 Homolog
- From:
Acta Physiologica Sinica
2023;75(1):59-68
- CountryChina
- Language:Chinese
-
Abstract:
The purpose of this study was to explore the effect and mechanism of dihydromyricetin (DHM) on Parkinson's disease (PD)-like lesions in type 2 diabetes mellitus (T2DM) rats. The T2DM model was established by feeding Sprague Dawley (SD) rats with high-fat diet and intraperitoneal injection of streptozocin (STZ). The rats were intragastrically administered with DHM (125 or 250 mg/kg per day) for 24 weeks. The motor ability of the rats was measured by balance beam experiment, the changes of dopaminergic (DA) neurons and the expression of autophagy initiation related protein ULK1 in the midbrains of the rats were detected by immunohistochemistry, and the protein expression levels of α-synuclein (α-syn), tyrosine hydroxylase (TH), as well as AMPK activation level, in the midbrains of the rats were detected by Western blot. The results showed that, compared with normal control, the rats with long-term T2DM exhibited motor dysfunction, increased α-syn aggregation, down-regulated TH protein expression, decreased number of DA neurons, declined activation level of AMPK, and significantly down-regulated ULK1 expression in the midbrain. DHM (250 mg/kg per day) treatment for 24 weeks significantly improved the above PD-like lesions, increased AMPK activity, and up-regulated ULK1 protein expression in T2DM rats. These results suggest that DHM may improve PD-like lesions in T2DM rats by activating AMPK/ULK1 pathway.
