摘要
目的研究依达拉奉对脂多糖(LPS)诱导的帕金森病(PD)大鼠模型的保护作用及机制。方法大鼠黑质内立体定向注射14μg LPS建立PD大鼠模型。选取造模成功PD大鼠24只,随机分成大、小剂量组和未治疗组。3组大鼠分别接受不同剂量的依达拉奉注射液(5.0mg/kg,1.0mg/kg)或生理盐水;另外选取正常大鼠5只,作为正常对照组。注射4w后观察各组大鼠黑质酪氨酸羟化酶(TH)阳性细胞的数量以及超氧化物歧化酶(SOD)及丙二醛(MDA)表达变化。结果与未治疗组相比,依达拉奉大、小剂量组TH阳性细胞数显著增多,SOD表达也明显增多(P<0.05),MDA表达明显减少(P<0.05)。结论依达拉奉可能通过减少LPS诱导的自由基产生而对PD大鼠发挥神经保护作用。
Objective To explore the protective effect of the edaravone on dopaminergic neurons of the PD rats in- duced by lipopolysaccharide(LPS). Methods The rat model of PD was established after intranigral injection of 15p, g LPS. Twenty-four female PD rats were randomly divided into three groups with different injection dose of edaravone (5.0mg/kg, 1.0mg/kg) and the injection of saline as control. Five normal rats were set as normal group. On 28d, the num- ber of tyrosine hydroxylase (TH) positive neurons and superoxide dismutase (SOD) and malondialdehyde ( MDA ) in the sub- stantia nigra(SN)were observed. Results The TH positive neurons survived in the animals treated with edaravone were more than those of the saline group (P 〈 0.05 ). The SOD levers of edaravone groups was higher, while MDA level was lower than the saline group( P 〈 0.05 ). Conclusion Edaravone attenuates LPS-induced degeneration of rat substantia nigral dopaminergic neurons.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2011年第1期53-54,共2页
Journal of Apoplexy and Nervous Diseases
关键词
依达拉奉
脂多糖
帕金森病
大鼠
Edaravone
Lipopolysaccharide
Parkinsons' disease
Rat