Influence of simvastatin on dopaminergic neurons of lipopolysaccharide-induced rat model of Parkinson's disease
10.1016/S1995-7645(14)60189-9
- Author:
Tan WANG
1
;
Bei-Sha TANG
1
;
Tan WANG
2
;
Xiao-Wu CHEN
2
;
Tian ZHANG
2
;
Zhi-Bin CHEN
2
;
Xue-Bin CAO
3
;
Pei-Pei HUANG
3
Author Information
1. Department of Neurology, Xiangya Hospital, Central South University
2. Department of Neurology, Affiliated Hospital of Hainan Medical College
3. Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology
- Publication Type:Journal Article
- Keywords:
Astrocyte;
Lipopolysaccharide;
Parkinson's disease;
Simvastatin;
Tumor necrosis factor-alpha
- From:
Asian Pacific Journal of Tropical Medicine
2015;8(1):64-67
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the neuroprotective effects of simvastatin on lipopolysaccharide (LPS)-induced rat model of Parkinson's disease (PD) and the mechanisms involved. Methods: Hemiparkinsonian rat models were induced by stereotaxieal injection of LPS in the right substantia nigra compacta. After 2 weeks of simvastatin treatment, rotational behavior test was performed after the intraperitoneal injection of apomorphine. Expression of tyroxine hydroxylase (TH) and glial fibrillary acidic protein were analyzed through immunohistochemical staining of substantia nigra and striatum, and the level of TNF- α was evaluated using enzyme-linked immunosorbent assay. Results: Comparing with untreated group, behavioral symptoms of the rats were significantly less in the rats that received simvastatin treatment. The TH positive cell count in substantia nigra and striatum were significantly increased (. P<0.05) and TNF- α expression was significantly decreased (. P<0.05) in simvastatin group compared to untreated group. Conclusions: Simvastatin could effectively inhibit the activation of astrocytes, reduce TNF- α expression, and exert anti-inflammatory effects, and thus protect the dopaminergic neurons in substantia nigra and striatum of the rat model of PD.
