辛伐他汀对脂多糖诱导的帕金森病大鼠模型多巴胺能神经元的影响。
Influence of simvastatin on dopaminergic neurons of lipopolysaccharide-induced rat model of Parkinson's disease.
作者信息
Wang Tan, Cao Xue-Bin, Chen Xiao-Wu, Huang Pei-Pei, Zhang Tian, Chen Zhi-Bin, Tang Bei-Sha
机构信息
Department of Neurology, Xiangya Hospital, Central South University, Changsha 410008, China; Department of Neurology, Affiliated Hospital of Hainan Medical College, Haikou 570102, China.
Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 43022, China.
出版信息
Asian Pac J Trop Med. 2015 Jan;8(1):64-7. doi: 10.1016/S1995-7645(14)60189-9.
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.
目的
研究辛伐他汀对脂多糖（LPS）诱导的帕金森病（PD）大鼠模型的神经保护作用及其相关机制。
方法
通过立体定向注射LPS至右侧黑质致密部诱导半帕金森病大鼠模型。辛伐他汀治疗2周后，腹腔注射阿扑吗啡后进行旋转行为测试。通过黑质和纹状体的免疫组织化学染色分析酪氨酸羟化酶（TH）和胶质纤维酸性蛋白的表达，并使用酶联免疫吸附测定法评估肿瘤坏死因子-α（TNF-α）水平。
结果
与未治疗组相比，接受辛伐他汀治疗的大鼠行为症状明显减轻。与未治疗组相比，辛伐他汀组黑质和纹状体中TH阳性细胞计数显著增加（P<0.05），TNF-α表达显著降低（P<0.05）。
结论
辛伐他汀可有效抑制星形胶质细胞的活化，降低TNF-α表达，发挥抗炎作用，从而保护PD大鼠模型黑质和纹状体中的多巴胺能神经元。
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